Page last updated: 2024-11-07

aldosterone and Hypertension, Essential

aldosterone has been researched along with Hypertension, Essential in 96 studies

Research Excerpts

ExcerptRelevanceReference
"Angiotensin II receptor blockers (ARBs) have been widely used to treat hypertension and large-scale clinical studies have shown various benefits."9.22Changeover Trial of Azilsartan and Olmesartan Comparing Effects on the Renin-Angiotensin-Aldosterone System in Patients with Essential Hypertension after Cardiac Surgery (CHAOS Study). ( Arimoto, M; Hata, H; Osaka, S; Sakino, H; Sezai, A; Shiono, M; Yaoita, H, 2016)
"To study the development of microalbuminuria (MAU) in essential hypertension (EHT), we investigated the association of MAU with central blood pressure (CBP), direct renin concentration (DRC), plasma aldosterone (PA), and uric acid (UA)."8.31Central diastolic blood pressure, plasma aldosterone and uric acid are associated with microalbuminuria in essential hypertension: a case-control study. ( Chou, H; Li, J; Li, Y; Shi, L; Wei, M; Yang, N, 2023)
"We investigated the changes of serum PTH levels induced by oral captopril (50 mg) administration in patients with primary essential hypertension (EH) and with primary aldosteronism (PA) caused by bilateral adrenal hyperplasia (BAH) or aldosterone-producing adenoma (APA), the latter before and after adrenalectomy."7.91PTH Modulation by Aldosterone and Angiotensin II is Blunted in Hyperaldosteronism and Rescued by Adrenalectomy. ( Iacobone, M; Lenzini, L; Lerco, S; Maiolino, G; Prisco, S; Rossi, GP; Seccia, TM; Torresan, F; Vanderriele, PE, 2019)
" Anthropometric parameters and aldosterone, plasma renin activity, cortisol, cortisone, Homeostasis Model Assessment Insulin Resistance (HOMA-IR), high-sensitivity C-reactive protein, adiponectin, IL-6, plasminogen activator inhibitor type 1 levels and matrix metalloproteinase-9 and matrix metalloproteinase-2 (MMP-9 and MMP-2) activities were measured."7.83Cortisol/cortisone ratio and matrix metalloproteinase-9 activity are associated with pediatric primary hypertension. ( Aglony, M; Allende, F; Bancalari, R; Baudrand, R; Campino, C; Carvajal, CA; Fardella, CE; Fuentes, CA; García, H; García, L; Kalergis, AM; Lagos, CF; Loureiro, C; Martinez-Aguayo, A; Sanhueza, S; Solari, S; Tapia-Castillo, A; Valdivia, C; Vecchiola, A, 2016)
"Among patients with essential hypertension, circulating endogenous ouabain and Aldo are typically coelevated and their BP is salt-sensitive."7.83Endogenous ouabain and aldosterone are coelevated in the circulation of patients with essential hypertension. ( Brioni, E; Casamassima, N; Hamlyn, JM; Lanzani, C; Manunta, P; Messaggio, E; Simonini, M; Tentori, S; Zagato, L, 2016)
"The objective of this article is to measure serum dehydroepiandrosterone sulfate (DHEA-S) concentration in both genders with primary aldosteronism (PA)."7.81Serum dehydroepiandrosterone sulfate concentration is lower in women with primary aldosteronism. ( Chen, AH; Huang, TS; Li, HY; Lin, YH; Wu, VC, 2015)
" Determination of metanephrines by high-pressure liquid chromatography has been well established for the diagnosis of pheochromocytomas, demonstrating high sensitivity and specificity."7.78Plasma and urinary metanephrines determined by an enzyme immunoassay, but not serum chromogranin A for the diagnosis of pheochromocytoma in patients with adrenal mass. ( Deutschbein, T; Hinrichs, J; Mann, K; Petersenn, S; Schmidt, H; Unger, N; Walz, MK, 2012)
"Aldosterone has hypertrophic and profibrotic effects on the heart."5.91Serum aldosterone effect on left ventricular structure and diastolic function in essential hypertension. ( Al-Hashedi, EM; Juvenal, H; Mohammed, AA; Yu, J; Zhao, X, 2023)
"Essential hypertension is a pivotal risk factor for the development of cardiovascular disease (CVD)."5.62Aldosterone hyperreactivity to acute psychosocial stress induction in men with essential hypertension. ( Ehlert, U; Gideon, A; Sauter, C; von Känel, R; Wirtz, PH, 2021)
"Primary aldosteronism is recognized as the most frequent cause of secondary hypertension, and its screening is expected to become a routine evaluation in most patients with hypertension."5.56Renin-Angiotensin-Aldosterone System Triple-A Analysis for the Screening of Primary Aldosteronism. ( Buffolo, F; Burrello, J; Domenig, O; Monticone, S; Mulatero, P; Pecori, A; Poglitsch, M; Tetti, M, 2020)
"Aldosterone treatment enhanced mRNA expression of genes associated with inflammation and fibrosis and stimulated differentiation of 3T3-L1 and brown preadipocytes."5.48Inflammation and Fibrosis in Perirenal Adipose Tissue of Patients With Aldosterone-Producing Adenoma. ( Fan, C; Guan, M; Tan, W; Wang, L; Wei, Q; Wu, C; Wu, P; Xie, C; Xu, L; Xue, Y; Zhang, H; Zhang, J, 2018)
"Primary aldosteronism is affecting about 10% of hypertensive patients."5.48Criteria for diagnosing primary aldosteronism on the basis of liquid chromatography-tandem mass spectrometry determinations of plasma aldosterone concentration. ( Amar, L; Azizi, M; Baffalie, L; Baron, S; Blanchard, A; Faucard, C; Faucon, AL; Houillier, P; Pagny, JY; Travers, S, 2018)
"All primary aldosteronism patients were diagnosed by autonomous aldosterone secretion using confirmatory tests, and then divided into nPA (n = 130) and primary aldosteronism patients with high PAC (hPA: n = 162) using a PAC cutoff level of less than 443 pmol/l (16 ng/dl), representing the normal upper limit of PAC."5.46Plasma aldosterone level within the normal range is less associated with cardiovascular and cerebrovascular risk in primary aldosteronism. ( Hamasaki, T; Hashimoto, K; Hayashi, RD; Kajimoto, Y; Kitamura, T; Kouhara, H; Kurebayashi, S; Mukai, K; Murata, M; Nakao, M; Otsuki, M; Shimomura, I; Takeiri, S; Tamada, D; Yamamoto, T, 2017)
"Aldosterone has hypertrophic and profibrotic effects on the heart."5.42Plasma aldosterone and left ventricular diastolic function in treatment-naïve patients with hypertension: tissue-Doppler imaging study. ( Catena, C; Kraigher-Krainer, E; Pieske, B; Pilz, S; Sechi, LA; Tomaschitz, A; Verheyen, N, 2015)
"In 10 patients with primary aldosteronism, median supine ARRP was 298 (range 48-1222) and ARRD 34 (range 2."5.40Measurement of plasma renin concentration instead of plasma renin activity decreases the positive aldosterone-to-renin ratio tests in treated patients with essential hypertension. ( Bassani, N; Biganzoli, E; Gritti, A; Lonati, C; Morganti, A, 2014)
"Angiotensin II receptor blockers (ARBs) have been widely used to treat hypertension and large-scale clinical studies have shown various benefits."5.22Changeover Trial of Azilsartan and Olmesartan Comparing Effects on the Renin-Angiotensin-Aldosterone System in Patients with Essential Hypertension after Cardiac Surgery (CHAOS Study). ( Arimoto, M; Hata, H; Osaka, S; Sakino, H; Sezai, A; Shiono, M; Yaoita, H, 2016)
"This exploratory study reports two plausible loci associated with SBP response to hydrochlorothiazide: TET2, an aldosterone-responsive mediator of αENaC gene transcription; and CSMD1, previously described as associated with hypertension in a case-control study."5.20TET2 and CSMD1 genes affect SBP response to hydrochlorothiazide in never-treated essential hypertensives. ( Argiolas, G; Barlassina, C; Boerwinkle, E; Braga, D; Carpini, SD; Chapman, AB; Chittani, M; Citterio, L; Condorelli, G; Cooper-Dehoff, RM; Cusi, D; Dominiczak, AF; Donner, KM; Frau, F; Fresu, G; Glorioso, N; Glorioso, V; Gong, Y; Hiltunen, TP; Johnson, JA; Kontula, KK; Lanzani, C; Manunta, P; Melander, O; Ortu, MF; Padmanabhan, S; Piras, DA; Pozzoli, S; Rivera, NV; Salvi, E; Simonini, M; Trimarco, B; Troffa, C; Turner, ST; Velayutham, D; Zaninello, R, 2015)
"To study the development of microalbuminuria (MAU) in essential hypertension (EHT), we investigated the association of MAU with central blood pressure (CBP), direct renin concentration (DRC), plasma aldosterone (PA), and uric acid (UA)."4.31Central diastolic blood pressure, plasma aldosterone and uric acid are associated with microalbuminuria in essential hypertension: a case-control study. ( Chou, H; Li, J; Li, Y; Shi, L; Wei, M; Yang, N, 2023)
"We investigated the changes of serum PTH levels induced by oral captopril (50 mg) administration in patients with primary essential hypertension (EH) and with primary aldosteronism (PA) caused by bilateral adrenal hyperplasia (BAH) or aldosterone-producing adenoma (APA), the latter before and after adrenalectomy."3.91PTH Modulation by Aldosterone and Angiotensin II is Blunted in Hyperaldosteronism and Rescued by Adrenalectomy. ( Iacobone, M; Lenzini, L; Lerco, S; Maiolino, G; Prisco, S; Rossi, GP; Seccia, TM; Torresan, F; Vanderriele, PE, 2019)
"Among patients with essential hypertension, circulating endogenous ouabain and Aldo are typically coelevated and their BP is salt-sensitive."3.83Endogenous ouabain and aldosterone are coelevated in the circulation of patients with essential hypertension. ( Brioni, E; Casamassima, N; Hamlyn, JM; Lanzani, C; Manunta, P; Messaggio, E; Simonini, M; Tentori, S; Zagato, L, 2016)
" Anthropometric parameters and aldosterone, plasma renin activity, cortisol, cortisone, Homeostasis Model Assessment Insulin Resistance (HOMA-IR), high-sensitivity C-reactive protein, adiponectin, IL-6, plasminogen activator inhibitor type 1 levels and matrix metalloproteinase-9 and matrix metalloproteinase-2 (MMP-9 and MMP-2) activities were measured."3.83Cortisol/cortisone ratio and matrix metalloproteinase-9 activity are associated with pediatric primary hypertension. ( Aglony, M; Allende, F; Bancalari, R; Baudrand, R; Campino, C; Carvajal, CA; Fardella, CE; Fuentes, CA; García, H; García, L; Kalergis, AM; Lagos, CF; Loureiro, C; Martinez-Aguayo, A; Sanhueza, S; Solari, S; Tapia-Castillo, A; Valdivia, C; Vecchiola, A, 2016)
"Thirty-three consecutive patients with essential hypertension and hypovitaminosis D underwent therapy with cholecalciferol 50 000 IU/week orally for 8 weeks."3.83Cholecalciferol treatment downregulates renin-angiotensin system and improves endothelial function in essential hypertensive patients with hypovitaminosid D. ( Bacca, A; Bernini, G; Bruno, RM; Carrara, D; Duranti, E; Ghiadoni, L; Taddei, S, 2016)
"The objective of this article is to measure serum dehydroepiandrosterone sulfate (DHEA-S) concentration in both genders with primary aldosteronism (PA)."3.81Serum dehydroepiandrosterone sulfate concentration is lower in women with primary aldosteronism. ( Chen, AH; Huang, TS; Li, HY; Lin, YH; Wu, VC, 2015)
"Urinary 18-hydroxycortisol has been investigated as a marker of aldosterone-producing adenoma (APA)."3.79Quantification of urinary 18-hydroxycortisol using LC-MS/MS. ( Chiba, H; Fuda, H; Fujikawa, M; Hui, SP; Ikegawa, S; Jin, S; Kurosawa, T; Sakurai, T; Takahashi, Y; Takeda, S; Wada, N; Yanagisawa, K, 2013)
" Determination of metanephrines by high-pressure liquid chromatography has been well established for the diagnosis of pheochromocytomas, demonstrating high sensitivity and specificity."3.78Plasma and urinary metanephrines determined by an enzyme immunoassay, but not serum chromogranin A for the diagnosis of pheochromocytoma in patients with adrenal mass. ( Deutschbein, T; Hinrichs, J; Mann, K; Petersenn, S; Schmidt, H; Unger, N; Walz, MK, 2012)
"Primary aldosteronism is associated with an increased risk of cardiovascular disease and kidney dysfunction compared to essential hypertension."3.01The Effect of Aldosterone on Cardiorenal and Metabolic Systems. ( Abe, M; Kobayashi, H; Otsuka, H, 2023)
"Aldosterone has hypertrophic and profibrotic effects on the heart."1.91Serum aldosterone effect on left ventricular structure and diastolic function in essential hypertension. ( Al-Hashedi, EM; Juvenal, H; Mohammed, AA; Yu, J; Zhao, X, 2023)
"Essential hypertension is a major disease, mostly with unknown underlying mechanisms."1.62Modulation of 11β-hydroxysteroid dehydrogenase functions by the cloud of endogenous metabolites in a local microenvironment: The glycyrrhetinic acid-like factor (GALF) hypothesis. ( Brem, AS; Morris, DJ; Odermatt, A, 2021)
"Patients with primary aldosteronism (PA) have cardiac remodeling due to hemodynamic and non-hemodynamic causes."1.62Hemodynamic and Non-Hemodynamic Components of Cardiac Remodeling in Primary Aldosteronism. ( Chang, CC; Chang, YR; Chang, YY; Chen, YL; Chen, ZW; Hung, CS; Lee, BC; Liao, CW; Lin, LC; Lin, YH; Pan, CT; Tsai, CH; Wu, XM, 2021)
"Essential hypertension is a pivotal risk factor for the development of cardiovascular disease (CVD)."1.62Aldosterone hyperreactivity to acute psychosocial stress induction in men with essential hypertension. ( Ehlert, U; Gideon, A; Sauter, C; von Känel, R; Wirtz, PH, 2021)
"Primary aldosteronism is recognized as the most frequent cause of secondary hypertension, and its screening is expected to become a routine evaluation in most patients with hypertension."1.56Renin-Angiotensin-Aldosterone System Triple-A Analysis for the Screening of Primary Aldosteronism. ( Buffolo, F; Burrello, J; Domenig, O; Monticone, S; Mulatero, P; Pecori, A; Poglitsch, M; Tetti, M, 2020)
"Primary aldosteronism (PA) is hemodynamically independently associated with arterial wall stiffness as assessed by pulse wave velocity (PWV) compared with essential hypertension."1.51Aldosterone Induces Vascular Damage. ( Chang, CC; Chen, CH; Chen, ZW; Cheng, HM; Hung, CS; Liao, CW; Lin, YH; Pan, CT; Sung, SH; Wu, VC, 2019)
"Primary aldosteronism is affecting about 10% of hypertensive patients."1.48Criteria for diagnosing primary aldosteronism on the basis of liquid chromatography-tandem mass spectrometry determinations of plasma aldosterone concentration. ( Amar, L; Azizi, M; Baffalie, L; Baron, S; Blanchard, A; Faucard, C; Faucon, AL; Houillier, P; Pagny, JY; Travers, S, 2018)
"The diagnosis of primary aldosteronism typically requires at least one confirmatory test."1.48Confirmatory Tests for the Diagnosis of Primary Aldosteronism: A Prospective Diagnostic Accuracy Study. ( Bruemmer, D; Cheng, Q; He, W; Hu, J; Li, Q; Luo, T; Ma, L; Mei, M; Peng, B; Qing, H; Song, Y; Wang, Y; Wang, Z; Yang, S; Zhang, S; Zhen, Q, 2018)
"Aldosterone treatment enhanced mRNA expression of genes associated with inflammation and fibrosis and stimulated differentiation of 3T3-L1 and brown preadipocytes."1.48Inflammation and Fibrosis in Perirenal Adipose Tissue of Patients With Aldosterone-Producing Adenoma. ( Fan, C; Guan, M; Tan, W; Wang, L; Wei, Q; Wu, C; Wu, P; Xie, C; Xu, L; Xue, Y; Zhang, H; Zhang, J, 2018)
"Primary aldosteronism is associated with a higher incidence of left ventricular (LV) hypertrophy and diastolic dysfunction than essential hypertension."1.48Aldosterone induces left ventricular subclinical systolic dysfunction: a strain imaging study. ( Chang, YY; Chen, CW; Chen, ZW; Huang, KC; Hung, CS; Lee, JK; Liao, CW; Lin, LC; Lin, YH; Wu, VC, 2018)
"Vascular function, including reactive hyperemia index (RIH), flow-mediated vasodilation (FMD), and nitroglycerine-induced vasodilation (NID) were evaluated in 52 patients with IHA, 53 patients with aldosterone-producing adenoma (APA), and 52 age-, sex-, and blood pressure-matched patients with essential hypertension (EHT)."1.48Microvascular endothelial function is impaired in patients with idiopathic hyperaldosteronism. ( Hashimoto, H; Higashi, Y; Kajikawa, M; Kihara, Y; Kishimoto, S; Maruhashi, T; Matsui, S; Matsumoto, T; Oki, K; Yusoff, FM, 2018)
"A total of 62 primary aldosteronism and 56 essential hypertension patients were enrolled."1.46Increased urinary excretion of the epithelial Na channel activator prostasin in patients with primary aldosteronism. ( Castagna, A; Chiariello, C; Chiecchi, L; Morandini, F; Olivieri, O; Pattini, P; Pizzolo, F; Salvagno, G; Zaltron, C; Zorzi, F, 2017)
"All primary aldosteronism patients were diagnosed by autonomous aldosterone secretion using confirmatory tests, and then divided into nPA (n = 130) and primary aldosteronism patients with high PAC (hPA: n = 162) using a PAC cutoff level of less than 443 pmol/l (16 ng/dl), representing the normal upper limit of PAC."1.46Plasma aldosterone level within the normal range is less associated with cardiovascular and cerebrovascular risk in primary aldosteronism. ( Hamasaki, T; Hashimoto, K; Hayashi, RD; Kajimoto, Y; Kitamura, T; Kouhara, H; Kurebayashi, S; Mukai, K; Murata, M; Nakao, M; Otsuki, M; Shimomura, I; Takeiri, S; Tamada, D; Yamamoto, T, 2017)
"To investigate the diagnostic value of plasma aldosterone-to-active-renin ratio(ARR)in combination with plasma aldosterone concentration(PAC)in the predication of aldosteronoma(APA)."1.43[An evaluation of plasma aldosterone-to-active-renin ratio in different postures in combination with aldosterone concentration in the diagnosis of aldosteronoma]. ( Ba, JM; Dou, JT; Gu, WJ; Guo, QH; Jin, N; Lyu, ZH; Mu, YM; Wang, XL; Yang, GQ; Yang, LJ; Zang, L; Zhu, J, 2016)
"Little is known about the prevalence of Liddle syndrome."1.42Prevalence of Liddle Syndrome Among Young Hypertension Patients of Undetermined Cause in a Chinese Population. ( Bian, J; Hui, RT; Jiang, XJ; Liu, YX; Song, L; Wang, LP; Wu, HY; Yang, KQ; Zhang, HM; Zhou, XL; Zou, YB, 2015)
"Although primary aldosteronism is associated with more prominent cardiac remodeling and diastolic dysfunction, the reversibility of diastolic function is unclear."1.42Circulating tissue inhibitor of matrix metalloproteinase-1 is associated with aldosterone-induced diastolic dysfunction. ( Chang, YS; Chang, YY; Chen, MF; Chen, YH; Chou, CH; Ho, YL; Hung, CS; Lin, YH; Su, MJ; Tsai, YC; Wu, KD; Wu, VC; Wu, XM, 2015)
"Aldosterone suppression was assessed in 73 essential hypertensive and 46 primary aldosteronism patients."1.42Clinical validation for the aldosterone-to-renin ratio and aldosterone suppression testing using simultaneous fully automated chemiluminescence immunoassays. ( Bidlingmaier, M; Diederich, S; Dietz, A; Fischer, E; Grimminger, P; Holmes, D; Junnila, R; Manolopoulou, J; Morganti, A; Reincke, M, 2015)
"Aldosterone has hypertrophic and profibrotic effects on the heart."1.42Plasma aldosterone and left ventricular diastolic function in treatment-naïve patients with hypertension: tissue-Doppler imaging study. ( Catena, C; Kraigher-Krainer, E; Pieske, B; Pilz, S; Sechi, LA; Tomaschitz, A; Verheyen, N, 2015)
"Primary aldosteronism and particularly its most caricatural form, that is APA, seems associated with a lower level of prorenin than essential hypertension."1.42Decreased plasma prorenin levels in primary aldosteronism: potential diagnostic implications. ( Berge, C; Bricca, G; Courand, PY; Fauvel, JP; Harbaoui, B; Khettab, F; Lantelme, P; Paget, V, 2015)
"Primary aldosteronism (PA), the most frequent form of secondary hypertension, is characterized by a higher rate of cardiovascular (CV) events than essential hypertension (EH)."1.40Primary aldosteronism and essential hypertension: assessment of cardiovascular risk at diagnosis and after treatment. ( Boscaro, M; Ceccoli, L; di Tizio, V; Giacchetti, G; Ronconi, V; Turchi, F, 2014)
"Patients with primary aldosteronism showed significant increase of NADPH oxidase (Nox2-dp) plasma levels and urinary isoprostanes (34."1.40Oxidative stress in patients affected by primary aldosteronism. ( Carnevale, R; Concistrè, A; De Toma, G; Letizia, C; Marinelli, C; Petramala, L; Pignatelli, P; Settevendemmie, A; Tonnarini, G; Violi, F; Zinnamosca, L, 2014)
"In 10 patients with primary aldosteronism, median supine ARRP was 298 (range 48-1222) and ARRD 34 (range 2."1.40Measurement of plasma renin concentration instead of plasma renin activity decreases the positive aldosterone-to-renin ratio tests in treated patients with essential hypertension. ( Bassani, N; Biganzoli, E; Gritti, A; Lonati, C; Morganti, A, 2014)

Research

Studies (96)

TimeframeStudies, this research(%)All Research%
pre-199017 (17.71)18.7374
1990's0 (0.00)18.2507
2000's0 (0.00)29.6817
2010's55 (57.29)24.3611
2020's24 (25.00)2.80

Authors

AuthorsStudies
Morris, DJ1
Brem, AS1
Odermatt, A1
Petramala, L3
Concistrè, A3
Circosta, F1
Gigante, A1
Sarlo, F1
Schina, M1
Soldini, M1
Iannucci, G2
Cianci, R1
Letizia, C3
McNally, RJ1
Morselli, F1
Farukh, B1
Chowienczyk, PJ1
Faconti, L1
Chen, PT2
Chang, D1
Liu, KL2
Liao, WC1
Wang, W2
Chang, CC5
Wu, VC10
Lin, YH11
Chang, CM1
Peng, KY2
Chan, CK2
Lin, YF1
Liao, HW1
Chang, JG1
Wu, MS1
Chang, WC1
Han, L1
Xu, XJ1
Zhang, JS1
Liu, HM1
Hu, YH2
Lai, TS1
Wang, SM2
Lu, CC1
Liu, YC1
Tsai, YC3
Chueh, JS1
Al-Hashedi, EM1
Zhao, X1
Mohammed, AA1
Juvenal, H1
Yu, J1
Gomez-Sanchez, CE1
Gomez-Sanchez, EP1
Otsuka, H2
Abe, M2
Kobayashi, H4
Kishimoto, S2
Oki, K2
Maruhashi, T2
Kajikawa, M2
Mizobuchi, A1
Harada, T1
Yamaji, T1
Hashimoto, Y1
Yoshimura, K1
Nakano, Y1
Goto, C1
Yusoff, FM2
Nakashima, A1
Higashi, Y3
Li, J2
Yang, N1
Chou, H1
Shi, L2
Wei, M1
Li, Y2
Burrello, J1
Buffolo, F1
Domenig, O1
Tetti, M1
Pecori, A1
Monticone, S1
Poglitsch, M1
Mulatero, P1
Libianto, R1
Fuller, PJ1
Young, MJ1
Yang, J1
Liu, Y2
Lin, Y1
Zhang, MM1
Li, XH1
Liu, YY1
Zhao, J1
Zhang, SL1
Gao, JW1
Guo, Y1
Feng, QL1
Tang, JY1
Yan, L1
Wang, JF1
Cheng, H1
Liu, PM1
Fuss, CT1
Brohm, K1
Kurlbaum, M1
Hannemann, A1
Kendl, S1
Fassnacht, M1
Deutschbein, T2
Hahner, S1
Kroiss, M1
Chu, HT1
Li, L1
Jia, M1
Diao, LL1
Li, ZB1
van der Heijden, CDCC1
Smeets, EMM1
Aarntzen, EHJG1
Wesseling, M1
de Jager, SCA1
Riksen, NP1
Teruyama, K1
Naruse, M2
Tsuiki, M1
Pan, CT2
Wu, XM4
Tsai, CH1
Chang, YY5
Chen, ZW3
Lee, BC2
Liao, CW4
Chen, YL1
Lin, LC2
Chang, YR1
Hung, CS6
Gideon, A1
Sauter, C1
Ehlert, U1
von Känel, R1
Wirtz, PH1
Chen, KM1
Lin, KH1
Wu, TH1
Hong, JS1
Moon, SJ1
Jang, HN1
Kim, JH1
Moon, MK1
Ruilope, LM1
Tamargo, J1
Spannella, F1
Giulietti, F1
Balietti, P1
Borioni, E1
Lombardi, FE1
Ricci, M1
Cocci, G1
Landi, L1
Sarzani, R1
Haase, M1
Dringenberg, T1
Allelein, S1
Willenberg, HS1
Schott, M1
Huang, KC1
Lee, JK2
Chen, CW2
Wu, C1
Zhang, H2
Zhang, J2
Xie, C1
Fan, C1
Wu, P1
Wei, Q1
Tan, W1
Xu, L1
Wang, L1
Xue, Y1
Guan, M1
Song, Y2
Yang, S2
He, W2
Hu, J2
Cheng, Q2
Wang, Y1
Luo, T1
Ma, L1
Zhen, Q2
Zhang, S1
Mei, M1
Wang, Z2
Qing, H1
Bruemmer, D1
Peng, B1
Li, Q2
Meng, X1
Wang, X1
Yu, Y1
Chou, CH2
Wei, LH1
Shun, CT1
Wen, WF1
Wan, CH1
Wu, KD4
Baron, S1
Amar, L1
Faucon, AL1
Blanchard, A1
Baffalie, L1
Faucard, C1
Travers, S1
Pagny, JY1
Azizi, M1
Houillier, P1
Davogustto, G1
Wang, TJ1
Gupta, DK1
Ohno, Y1
Sone, M1
Inagaki, N1
Yamasaki, T1
Ogawa, O1
Takeda, Y1
Kurihara, I1
Umakoshi, H1
Ichijo, T1
Katabami, T1
Wada, N2
Ogawa, Y1
Yoshimoto, T1
Kawashima, J1
Watanabe, M1
Matsuda, Y1
Shibata, H1
Miyauchi, S1
Kamemura, K1
Fukuoka, T1
Yamamoto, K1
Otsuki, M2
Suzuki, T1
Matsumoto, T1
Matsui, S1
Hashimoto, H1
Kihara, Y2
Lenzini, L1
Prisco, S1
Vanderriele, PE1
Lerco, S1
Torresan, F1
Maiolino, G1
Seccia, TM1
Iacobone, M1
Rossi, GP1
Bisogni, V1
Mezzadri, M1
Olmati, F1
Saracino, V1
Oliviero, G1
Bonvicini, M1
Tonnarini, G2
Sung, SH1
Chen, CH1
Cheng, HM1
McQuarrie, EP1
Freel, EM1
Mark, PB1
Fraser, R1
Connell, JM1
Jardine, AG1
Tzamou, V1
Vyssoulis, G1
Karpanou, E1
Kyvelou, SM1
Gialernios, T1
Stefanadis, C1
Chen, AH1
Li, HY1
Huang, TS1
Ceccoli, L2
Ronconi, V2
Giovannini, L1
Marcheggiani, M1
Turchi, F2
Boscaro, M2
Giacchetti, G2
Wu, CH1
Yang, YW1
Kuo, KL1
Hung, SC1
Jin, S1
Takahashi, Y1
Hui, SP1
Sakurai, T1
Fuda, H1
Takeda, S1
Fujikawa, M1
Yanagisawa, K1
Ikegawa, S1
Kurosawa, T1
Chiba, H1
Schumacher, CD1
Steele, RE1
Brunner, HR1
He, YB1
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Bassani, N1
Gritti, A1
Biganzoli, E1
Morganti, A2
Liu, YZ1
Wu, JJ1
Zhang, L1
Xu, H1
Liu, Z1
Lu, JP1
Feng, L1
Guo, Q1
Zhao, CM1
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Wei, H1
Cao, S1
Zhao, H1
Pilz, S3
Kienreich, K1
Gaksch, M2
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Verheyen, N3
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Schmid, J1
Drechsler, C1
Ritz, E2
Moosbrugger, A1
Stepan, V1
Pieber, TR1
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Tomaschitz, A3
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Pieske, B2
Wiecek, A1
Rus-Machan, J1
Toplak, H1
Amrein, K1
Kraigher-Krainer, E2
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Lee, HH1
Liao, MT1
Chen, YH2
Pignatelli, P1
Carnevale, R1
Zinnamosca, L1
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De Toma, G1
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Courand, PY1
Harbaoui, B1
Paget, V1
Khettab, F1
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Fauvel, JP1
Lantelme, P1
Chittani, M1
Zaninello, R1
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Ortu, MF1
Salvi, E1
Fresu, G1
Citterio, L1
Braga, D1
Piras, DA1
Carpini, SD1
Velayutham, D1
Simonini, M2
Argiolas, G1
Pozzoli, S1
Troffa, C1
Glorioso, V1
Kontula, KK1
Hiltunen, TP1
Donner, KM1
Turner, ST1
Boerwinkle, E1
Chapman, AB1
Padmanabhan, S1
Dominiczak, AF1
Melander, O1
Johnson, JA1
Cooper-Dehoff, RM1
Gong, Y1
Rivera, NV1
Condorelli, G1
Trimarco, B1
Manunta, P2
Cusi, D1
Glorioso, N1
Barlassina, C1
Catena, C2
Sechi, LA2
Markou, A1
Sertedaki, A1
Kaltsas, G1
Androulakis, II1
Marakaki, C1
Pappa, T1
Gouli, A1
Papanastasiou, L1
Fountoulakis, S1
Zacharoulis, A1
Karavidas, A1
Ragkou, D1
Charmandari, E1
Chrousos, GP1
Piaditis, GP1
Titov, VN1
Cho, JS1
Ihm, SH1
Kim, CJ1
Park, MW1
Her, SH1
Park, GM1
Kim, TS1
Wang, LP1
Yang, KQ1
Jiang, XJ1
Wu, HY1
Zhang, HM1
Zou, YB1
Song, L1
Bian, J1
Hui, RT1
Liu, YX1
Zhou, XL1
Chang, YS1
Su, MJ1
Ho, YL1
Chen, MF1
Manolopoulou, J1
Fischer, E1
Dietz, A1
Diederich, S1
Holmes, D1
Junnila, R1
Grimminger, P1
Reincke, M1
Bidlingmaier, M1
Colussi, G1
Brosolo, G1
Novello, M1
Jiang, Y1
Zhang, C1
Ye, L1
Su, T1
Zhou, W1
Jiang, L1
Zhang, Y1
Long, J1
Feng, Z1
Li, R1
Ren, W1
Zhou, B1
Sezai, A1
Osaka, S1
Yaoita, H1
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Hata, H1
Shiono, M1
Sakino, H1
Zhu, J1
Jin, N1
Zang, L1
Gu, WJ1
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Lagos, CF1
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Bruno, RM1
Bacca, A2
Taddei, S2
Duranti, E2
Ghiadoni, L2
Bernini, G2
Pizzolo, F1
Chiecchi, L1
Morandini, F1
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Zaltron, C1
Pattini, P1
Chiariello, C1
Salvagno, G1
Olivieri, O1
Armanini, D1
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Ambrosini, G1
Bordin, L1
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Haketa, A1
Takahiro, U1
Tanaka, S1
Hatanaka, Y1
Ikeda, Y1
Fukuda, N1
Soma, M1
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Kitamura, T1
Tamada, D1
Mukai, K1
Kurebayashi, S1
Yamamoto, T1
Hashimoto, K1
Hayashi, RD1
Kouhara, H1
Takeiri, S1
Kajimoto, Y1
Nakao, M1
Hamasaki, T1
Shimomura, I1
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Schmidt, H1
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Petersenn, S1
Kisaka, T1
Ozono, R1
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HARNAGEA, P1
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CROXATTO, R1
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GONZALEZ, J1
SCHAEFER, HE1
WOELFER, HJ1
SCHNEIDER, KW1

Clinical Trials (8)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
LC-MS/MS-specific Cutoffs for Screening and Confirmatory Testing of Primary Aldosteronism: A Multi-center Study[NCT05959863]300 participants (Anticipated)Observational2023-08-30Recruiting
A Phase II, Randomized, Double-blind, Placebo Controlled, Multi-center Study to Evaluate the Effects of LCI699 on Cortisol in Patients With Hypertension[NCT00817414]Phase 263 participants (Actual)Interventional2009-01-14Completed
A Multi-center, Randomized, Double-blind, Placebo and Active Controlled, Parallel Group, Dose Finding Study to Evaluate the Efficacy and Safety of LCI699 Compared to Placebo After 8 Weeks Treatment in Patients With Essential Hypertension[NCT00758524]Phase 2628 participants (Actual)Interventional2008-09-11Completed
A Phase II, Randomized, Double-blind, Placebo and Active Controlled, Parallel Group, Multi-center, Dose Ranging Study to Evaluate the Efficacy and Safety of LCI699 Compared to Placebo After 8 Weeks Treatment in Patients With Resistant Hypertension[NCT00817635]Phase 2155 participants (Actual)Interventional2008-12-22Completed
A Pilot, Single-blind, Forced-titration Study to Assess the Hemodynamic and Hormonal Effects, Safety and Tolerability of the Aldosterone Synthase Inhibitor LCI699 in Patients With Primary Hyperaldosteronism[NCT00732771]Phase 212 participants (Anticipated)Interventional2008-06-30Completed
Increasing Stay-on-therapy in Hypertensive Patients Treated With First-line Diuretics: An Active Pharmacosurveillance and Pharmacogenetic Study.[NCT00408512]Phase 42,500 participants (Anticipated)Interventional2006-12-31Completed
Hypertension in High School Students: Genetic and Environmental Factors[NCT06049641]2,638 participants (Actual)Observational2014-10-31Completed
Technology Assisted Management of Uncontrolled Hypertension (TEAM-HTN): a Pilot Study[NCT03281772]180 participants (Anticipated)Observational2017-01-24Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Apparent Terminal Half-life (T1/2) of LCI699

(NCT00817414)
Timeframe: Days 7, 28: Pre-dose and 3 hours post-dose; Day 30: Pre-dose; Day 42: Pre-dose and 0.5, 1, 2, 3, 4, and 8-hours post-dose

Interventionhr (Geometric Mean)
Cohort A: LCI699 0.5 mg QD4.67
Cohort A: LCI699 1.0 mg QD3.79
Cohort B1: LCI699 1.0 mg BID5.52
Cohort B1: LCI699 2.0 mg QD4.90

Area Under the Concentration Time Curve From Time 0 to 8 Hours Post LCI699 Administration (AUC0-8)

(NCT00817414)
Timeframe: Day 42: Pre-dose and 0.5, 1, 2, 3, 4, and 8-hours post-dose

Interventionnanogram*hour per milliliter (ng*hr/mL) (Geometric Mean)
Cohort A: LCI699 0.5 mg QD6.60
Cohort A: LCI699 1.0 mg QD14.1
Cohort B1: LCI699 1.0 mg BID24.1
Cohort B1: LCI699 2.0 mg QD46.4

Area Under the Concentration Time Curve Over the Dosing Interval (AUC0-τ) for LCI699

(NCT00817414)
Timeframe: Days 7, 28: Pre-dose and 3 hours post-dose; Day 30: Pre-dose; Day 42: Pre-dose and 0.5, 1, 2, 3, 4, and 8-hours post-dose

Interventionng*hr/mL (Geometric Mean)
Cohort A: LCI699 0.5 mg QD9.23
Cohort A: LCI699 1.0 mg QD18.8
Cohort B1: LCI699 1.0 mg BID30.6
Cohort B1: LCI699 2.0 mg QD68.9

LCI699 Plasma Concentration Post LCI699 Administration at Day 7

(NCT00817414)
Timeframe: Predose and 3 hours post-dose on Day 7

Interventionnanogram per milliliter (ng/mL) (Geometric Mean)
Cohort A: LCI699 0.5 mg QD1.51
Cohort A: LCI699 1.0 mg QD2.88
Cohort B1: LCI699 1.0 mg BID3.92
Cohort B1: LCI699 2.0 mg QD6.73

Maximum Plasma Concentration (Cmax) of LCI699

(NCT00817414)
Timeframe: Days 7, 28: Pre-dose and 3 hours post-dose; Day 30: Pre-dose; Day 42: Pre-dose and 0.5, 1, 2, 3, 4, and 8-hours post-dose

Interventionng/mL (Geometric Mean)
Cohort A: LCI699 0.5 mg QD1.42
Cohort A: LCI699 1.0 mg QD2.94
Cohort B1: LCI699 1.0 mg BID4.62
Cohort B1: LCI699 2.0 mg QD8.86

Maximum Tolerated Dose (MTD) of LCI699 With Respect to Effect on the Adrenocorticotropic Hormone (ACTH)-Stimulated Cortisol Response Following ACTH Stimulation in Hypertensive Participants

As per the protocol, MTD is the dose at which 4 participants exhibited ACTH-stimulated cortisol results <400 nanomoles per liter (nmol/L). The change in the distribution across the treatments were analyzed using 1- way analysis of variance (ANOVA) for continuous variables. (NCT00817414)
Timeframe: Up to Week 6

Interventionmilligrams (mg) (Number)
LCI6991.30

Number of Participants With Adverse Event (AEs)

An AE is an adverse medical event which occurs in a participant of the study and which is not necessarily in a causal relationship with the treatment the participant receives. (NCT00817414)
Timeframe: Up to 8 weeks

InterventionParticipants (Count of Participants)
Cohort A: LCI699 0.5 mg QD6
Cohort A: LCI699 1 mg QD9
Cohort B1: LCI699 1 mg BID10
Cohort B1: LCI699 2 mg QD10
Placebo10

Time of Maximum Plasma Concentration (Tmax) of LCI699

(NCT00817414)
Timeframe: Days 7, 28: Pre-dose and 3 hours post-dose; Day 30: Pre-dose; Day 42: Pre-dose and 0.5, 1, 2, 3, 4, and 8-hours post-dose

Interventionhour (hr) (Median)
Cohort A: LCI699 0.5 mg QD2.21
Cohort A: LCI699 1.0 mg QD1.00
Cohort B1: LCI699 1.0 mg BID1.00
Cohort B1: LCI699 2.0 mg QD1.00

LCI699 Exposure-response Relationship on Cortisol Levels Following ACTH Stimulation in Hypertensive Participants

Exposure-response relationship was assessed using ACTH stimulation test. Tests were done 2 hours after study drug administration (i.e., at peak LCI699 concentrations). An increase in cortisol greater than >500 nmol at 60 minutes after ACTH administration was expected. (NCT00817414)
Timeframe: Up to Week 6

,,,,
Interventionnanomoles per liter (nmol/L) (Mean)
Day 7Day 28Day 42
Cohort A: LCI699 0.5 mg QD690.0634.87647.51
Cohort A: LCI699 1.0 mg QD669.40573.41626.08
Cohort B1: LCI699 1.0 mg BID625.06554.79539.68
Cohort B1: LCI699 2.0 mg QD562.04539.09479.91
Placebo799.06804.86812.91

Percentage of Participants With a Mean Sitting Diastolic Blood Pressure (MSDBP) Response and MSDBP Control at Week 6 LOCF, as Measured by OBP

Automated arterial BP determinations was made with an automated BP device (such as the Omron BP monitor) in accordance with the Guidelines for management of hypertension: report of the 4th working party of the British Hypertension Society, 2004-BHS IV. Sitting and standing BP and HR measurements were performed. MSDBP response was defined as the percentage of participants with a MSDBP <90 mmHg or a >= 10 mmHg reduction from baseline. MSDBP control was defined as the percentage of participants with a MSDBP <90 mmHg for non-diabetic participants and <80mHg for diabetic participants. (NCT00817414)
Timeframe: Week 6

,,,,
Interventionpercentage of participants (Number)
MSDBP ResponseMSDBP Control
Cohort A: LCI699 0.5 mg QD58.358.3
Cohort A: LCI699 1 mg QD66.766.7
Cohort B1: LCI699 1 mg BID10076.9
Cohort B1: LCI699 2 mg QD76.976.9
Placebo61.546.2

Percentage of Participants With a Mean Sitting Systolic Blood Pressure (MSSBP) Response and MSSBP Control at Week 6 Last Observation Carried Forward (LOCF), as Measured by Office Blood Pressure (OBP)

Automated arterial BP determinations was made with an automated BP device (such as the Omron BP monitor) in accordance with the Guidelines for management of hypertension: report of the 4th working party of the British Hypertension Society, 2004-BHS IV. Sitting and standing blood pressure (BP) and heart rate (HR) measurements were performed. MSSBP response was defined as the percentage of participants with a MSSBP <140 mmHg or a >=20 mmHg reduction from baseline. MSSBP control was defined as the percentage of participants with a MSSBP <140 mmHg for non-diabetic participants and <130mHg for diabetic participants. (NCT00817414)
Timeframe: Week 6

,,,,
Interventionpercentage of participants (Number)
MSSBP ResponseMSSBP Control
Cohort A: LCI699 0.5 mg QD58.350.0
Cohort A: LCI699 1 mg QD50.041.7
Cohort B1: LCI699 1 mg BID69.261.5
Cohort B1: LCI699 2 mg QD76.976.9
Placebo61.553.8

Core Period: Change From Baseline in Mean 24 Hour Ambulatory DBP at Week 8, as Measured by ABPM

An ABPM measured a participant's BP over a 24-hour period readings using an automated validated monitoring device from Baseline to Week 8. The 24-hour DBP was calculated by taking the mean of all ambulatory DBP readings for the 24-hour period. (NCT00758524)
Timeframe: Baseline, Week 8

Interventionmm Hg (Least Squares Mean)
Core Period: LCI699 0.25 mg QD-4.03
Core Period: LCI699 0.5 mg QD-2.44
Core Period: LCI699 1.0 mg QD-4.96
Core Period: LCI699 0.5 mg BID-2.75
Core Period: Eplerenone 50 mg BID-6.03
Core Period: Placebo1.03

Core Period: Change From Baseline in Mean 24 Hour Ambulatory SBP at Week 8 as Measured by Ambulatory Blood Pressure Monitoring (ABPM)

An ABPM measured a participant's BP over a 24-hour period readings using an automated validated monitoring device from Baseline to Week 8. The 24-hour SBP was calculated by taking the mean of all ambulatory SBP readings for the 24-hour period. (NCT00758524)
Timeframe: Baseline, Week 8

Interventionmm Hg (Least Squares Mean)
Core Period: LCI699 0.25 mg QD-7.15
Core Period: LCI699 0.5 mg QD-4.90
Core Period: LCI699 1.0 mg QD-7.73
Core Period: LCI699 0.5 mg BID-6.18
Core Period: Eplerenone 50 mg BID-10.52
Core Period: Placebo1.11

Core Period: Change From Baseline in Mean Sitting Diastolic Blood Pressure (MSDBP) at Week 8 Last Observation Carried Forward (LOCF), as Measured by Office Blood Pressure (OBP)

Automated arterial BP determinations were made after the participant was in the sitting position for 5 minutes according to the Guidelines for management of hypertension: report of the 4th working party of the British Hypertension Society, 2004-BHS IV, using an automated BP device (such as the Omron BP monitor). The change in the MSDBP was calculated comparing the Week 8 readings to the readings taken at Baseline. The change from baseline in MSDBP was analyzed using an analysis of covariance model (ANCOVA) with treatment and region as factors and baseline MSDBP level as a covariate. (NCT00758524)
Timeframe: Baseline, Week 8

Interventionmm Hg (Mean)
Core Period: LCI699 0.25 mg QD-4.47
Core Period: LCI699 0.5 mg QD-5.50
Core Period: LCI699 1.0 mg QD-7.11
Core Period: LCI699 0.5 mg BID-4.25
Core Period: Eplerenone 50 mg BID-7.49
Core Period: Placebo-3.22

Core Period: Change From Baseline in Mean Sitting Systolic Blood Pressure (MSSBP) at Week 8 LOCF, as Measured by OBP

Automated arterial BP determinations were made after the participant was in the sitting position for 5 minutes according to the Guidelines for management of hypertension: report of the 4th working party of the British Hypertension Society, 2004-BHS IV, using an automated BP device (such as the Omron BP monitor). The change in the MSSBP was calculated comparing the Week 8 readings to the readings taken at Baseline. The change from baseline in MSSBP was analyzed using an ANCOVA with treatment and region as factors and baseline MSSBP levels as a covariate. (NCT00758524)
Timeframe: Baseline, Week 8

Interventionmm Hg (Mean)
Core Period: LCI699 0.25 mg QD-9.00
Core Period: LCI699 0.5 mg QD-10.69
Core Period: LCI699 1.0 mg QD-11.93
Core Period: LCI699 0.5 mg BID-9.10
Core Period: Eplerenone 50 mg BID-13.31
Core Period: Placebo-2.93

Core Period: Change From Baseline in Plasma Aldosterone Levels at Week 8

Change from baseline was analyzed using plasma aldosterone values measured at Baseline and Week 8. (NCT00758524)
Timeframe: Baseline, Week 8

Interventionpicomoles per liter (pmol/L) (Mean)
Core Period: LCI699 0.25 mg QD-21.5
Core Period: LCI699 0.5 mg QD-20.0
Core Period: LCI699 1.0 mg QD-9.9
Core Period: LCI699 0.5 mg BID-47.5
Core Period: Eplerenone 50 mg BID277.1
Core Period: Placebo-28.8

Core Period: Change From Baseline in Plasma Cortisol Levels by Adrenocorticotropic Hormone (ACTH) Stimulation Test

The ACTH stimulation cortisol test was a standard procedure to measure the ability of adrenal cortex to respond to exogenous ACTH and directly assess the adrenal reserve. Serum cortisol concentrations at 1 hour after injection were measured to assess the maximum stimulated cortisol level achieved. Potential adrenal suppression was indicated if the serum cortisol concentration was <500 nanomoles per liter (nmol/L) at 1 hour after the injection. (NCT00758524)
Timeframe: Baseline, 1 hour post-dose at Week 8

Interventionnanomoles per liter (nmol/L) (Mean)
Core Period: LCI699 0.25 mg QD729.20
Core Period: LCI699 0.5 mg QD692.74
Core Period: LCI699 1.0 mg QD604.46
Core Period: LCI699 0.5 mg BID609.21
Core Period: Eplerenone 50 mg BID802.32
Core Period: Placebo822.65

Core Period: Dose Response Relationship of LCI699 as Measured by Change From Baseline in MSDBP at Week 8

Automated arterial BP determinations were made after the participant was in the sitting position for 5 minutes according to the Guidelines for management of hypertension: report of the 4th working party of the British Hypertension Society, 2004-BHS IV, using an automated BP device (such as the Omron BP monitor). The change in the MSDBP was calculated comparing the Week 8 readings to the readings taken at Baseline. The change from baseline in MSDBP was analyzed using an analysis of covariance model (ANCOVA) with treatment and region as factors and baseline MSDBP level as a covariate. (NCT00758524)
Timeframe: Baseline, Week 8

Interventionmm Hg (Mean)
Core Period: LCI699 0.25 mg QD-4.47
Core Period: LCI699 0.5 mg QD-5.50
Core Period: LCI699 1.0 mg QD-7.11
Core Period: LCI699 0.5 mg BID-4.25

Core Period: Dose Response Relationship of LCI699 as Measured by Change From Baseline in MSSBP at Week 8

Automated arterial BP determinations were made after the participant was in the sitting position for 5 minutes according to the Guidelines for management of hypertension: report of the 4th working party of the British Hypertension Society, 2004-BHS IV, using an automated BP device (such as the Omron BP monitor). The change in the MSSBP was calculated comparing the Week 8 readings to the readings taken at Baseline. The change from baseline in MSSBP was analyzed using an ANCOVA with treatment and region as factors and baseline MSSBP levels as a covariate. (NCT00758524)
Timeframe: Baseline, Week 8

Interventionmm Hg (Mean)
Core Period: LCI699 0.25 mg QD-9.00
Core Period: LCI699 0.5 mg QD-10.69
Core Period: LCI699 1.0 mg QD-11.93
Core Period: LCI699 0.5 mg BID-9.10

Withdrawal Period: Change From Week 8 to Week 9 in MSDBP at Week 9, as Measured by OBP

Automated arterial BP determinations were made after the participant was in the sitting position for 5 minutes according to the Guidelines for management of hypertension: report of the 4th working party of the British Hypertension Society, 2004-BHS IV, using an automated BP device (such as the Omron BP monitor). The change in the MSDBP was calculated comparing the Week 9 readings to the readings taken at Week 8 (Baseline). The change from Week 8 to week 9 in MSDBP was analyzed using an ANCOVA with treatment and region as factors and Week 8 MSDBP level as a covariate. (NCT00758524)
Timeframe: From Week 8 to Week 9

Interventionmm Hg (Least Squares Mean)
Withdrawal Period: LCI699 0.25 mg QD0.5
Withdrawal Period: LCI699 0.25 mg QD Placebo0.5
Withdrawal Period: LCI699 0.5 mg QD1.6
Withdrawal Period: LCI699 0.5 mg QD Placebo-0.2
Withdrawal Period: LCI699 1.0 mg QD-0.5
Withdrawal Period: LCI699 1.0 mg QD Placebo2.5
Withdrawal Period: LCI699 0.5 mg BID1.3
Withdrawal Period: LCI699 0.5 mg BID Placebo1.3
Withdrawal Period: Eplerenone 50 mg BID-1.2
Withdrawal Period: Eplerenone 50 mg BID Placebo0.4
Withdrawal Period: Placebo1.6

Withdrawal Period: Change From Week 8 to Week 9 in MSSBP at Week 9 as Measured by OBP

Automated arterial BP determinations were made after the participant was in the sitting position for 5 minutes according to the Guidelines for management of hypertension: report of the 4th working party of the British Hypertension Society, 2004-BHS IV, using an automated BP device (such as the Omron BP monitor). The change in the MSSBP was calculated comparing the Week 9 readings to the readings taken at Week 8 (Baseline). The change from Week 8 to week 9 in MSSBP was analyzed using an ANCOVA with treatment and region as factors and Week 8 MSSBP level as a covariate. (NCT00758524)
Timeframe: From Week 8 to Week 9

Interventionmm Hg (Least Squares Mean)
Withdrawal Period: LCI699 0.25 mg QD0.3
Withdrawal Period: LCI699 0.25 mg QD Placebo3.3
Withdrawal Period: LCI699 0.5 mg QD0.5
Withdrawal Period: LCI699 0.5 mg QD Placebo2.5
Withdrawal Period: LCI699 1.0 mg QD0.4
Withdrawal Period: LCI699 1.0 mg QD Placebo5.3
Withdrawal Period: LCI699 0.5 mg BID1.6
Withdrawal Period: LCI699 0.5 mg BID Placebo4.4
Withdrawal Period: Eplerenone 50 mg BID-1.5
Withdrawal Period: Eplerenone 50 mg BID Placebo2.7
Withdrawal Period: Placebo1.8

Core Period: Number of Participants With Adverse Event (AEs), Serious Adverse Events (SAEs), and Deaths

An AE was an adverse medical event which occurs in a participant of the study and which is not necessarily in a causal relationship with the treatment the participant receives. SAEs were AEs leading to death, are life-threatening, require hospitalizations or prolongation of hospitalizations, represent an innate malformation or a congenital abnormality. (NCT00758524)
Timeframe: AEs: From start of the study drug treatment up to 8 weeks; SAE: From signing of the informed consent up to 8 weeks

,,,,,
InterventionParticipants (Count of Participants)
AEsSAEsDeaths
Core Period: Eplerenone 50 mg BID2600
Core Period: LCI699 0.25 mg QD2310
Core Period: LCI699 0.5 mg BID2700
Core Period: LCI699 0.5 mg QD2200
Core Period: LCI699 1.0 mg QD2400
Core Period: Placebo2310

Core Period: Percentage of Participants With a MSDBP Response and MSDBP Control at Week 8 LOCF

MSDBP response was defined as the percentage of participants with a MSDBP <90 mmHg or a >=10 mmHg reduction from Baseline. MSDBP control was defined as the percentage of participants with a MSDBP <90 mmHg. (NCT00758524)
Timeframe: Baseline, Week 8

,,,,,
Interventionpercentage of participants (Number)
MSDBP ResponseMSDBP Control
Core Period: Eplerenone 50 mg BID48.845.2
Core Period: LCI699 0.25 mg QD39.132.6
Core Period: LCI699 0.5 mg BID34.429.2
Core Period: LCI699 0.5 mg QD34.129.4
Core Period: LCI699 1.0 mg QD50.041.9
Core Period: Placebo27.618.4

Core Period: Percentage of Participants With a MSSBP Response and MSSBP Control at Week 8 LOCF

MSSBP response was defined as the percentage of participants with a MSSBP <140 mmHg or a >=20 mmHg reduction from baseline reduction from baseline. MSSBP control was defined as the percentage of participants with a MSSBP <140 mmHg. (NCT00758524)
Timeframe: Baseline, Week 8

,,,,,
Interventionpercentage of participants (Number)
MSSBP ResponseMSSBP Control
Core Period: Eplerenone 50 mg BID52.444.0
Core Period: LCI699 0.25 mg QD39.131.5
Core Period: LCI699 0.5 mg BID34.425.0
Core Period: LCI699 0.5 mg QD37.627.1
Core Period: LCI699 1.0 mg QD48.840.7
Core Period: Placebo17.115.8

Core Period: Trough to Hour Ratio for Change From Baseline in 24-hour Mean Ambulatory DBP at Week 8

Trough to peak ratios were derived from an ANCOVA model containing treatment, region, hour, treatment by hour interaction as factors with Baseline as a covariate. (NCT00758524)
Timeframe: Baseline, every hour up to 24 hours post-dose at Week 8

,,,,,
Interventionratio (Least Squares Mean)
Week 8, Hour 1Week 8, Hour 2Week 8, Hour 3Week 8, Hour 4Week 8, Hour 5Week 8, Hour 6Week 8, Hour 7Week 8, Hour 8Week 8, Hour 9Week 8, Hour 10Week 8, Hour 11Week 8, Hour 12Week 8, Hour 13Week 8, Hour 14Week 8, Hour 15Week 8, Hour 16Week 8, Hour 17Week 8, Hour 18Week 8, Hour 19Week 8, Hour 20Week 8, Hour 21Week 8, Hour 22Week 8, Hour 23Week 8, Hour 24
Core Period: Eplerenone 50 mg BID0.17-1.65-2.42-1.39-2.91-4.86-3.70-2.30-2.81-2.43-1.93-3.20-5.35-7.64-9.03-12.55-12.88-13.49-10.13-10.47-10.51-7.60-5.54-2.78
Core Period: LCI699 0.25 mg QD3.911.441.160.511.11-1.18-1.85-3.01-1.24-0.59-1.02-1.60-4.32-6.47-8.34-8.92-10.26-10.68-10.13-10.73-9.31-7.90-4.94-0.21
Core Period: LCI699 0.5 mg BID3.873.444.012.641.451.201.212.093.270.491.54-1.06-1.45-2.96-6.10-9.54-10.38-11.85-10.78-10.49-8.22-6.35-2.671.36
Core Period: LCI699 0.5 mg QD2.951.851.132.91-0.02-2.36-0.95-1.38-0.072.601.722.53-1.20-3.29-5.82-8.37-10.99-11.73-10.12-8.06-7.68-4.93-1.931.45
Core Period: LCI699 1.0 mg QD0.270.17-0.360.35-1.69-3.01-2.63-2.43-2.25-1.65-1.54-3.10-5.31-7.38-8.89-10.50-12.71-11.88-9.74-10.43-9.66-5.37-1.180.29
Core Period: Placebo7.116.284.997.024.311.823.622.653.303.862.383.241.52-0.90-1.01-1.61-4.20-6.89-5.84-5.21-4.12-1.091.821.98

Core Period: Trough to Hour Ratio for Change From Baseline in 24-hour Mean Ambulatory SBP at Week 8

Trough to peak ratios were derived from an ANCOVA model containing treatment, region, hour, treatment by hour interaction as factors with Baseline as a covariate. (NCT00758524)
Timeframe: Baseline, every hour up to 24 hours post-dose at Week 8

,,,,,
Interventionratio (Least Squares Mean)
Week 8, Hour 1Week 8, Hour 2Week 8, Hour 3Week 8, Hour 4Week 8, Hour 5Week 8, Hour 6Week 8, Hour 7Week 8, Hour 8Week 8, Hour 9Week 8, Hour 10Week 8, Hour 11Week 8, Hour 12Week 8, Hour 13Week 8, Hour 14Week 8, Hour 15Week 8, Hour 16Week 8, Hour 17Week 8, Hour 18Week 8, Hour 19Week 8, Hour 20Week 8, Hour 21Week 8, Hour 22Week 8, Hour 23Week 8, Hour 24
Core Period: Eplerenone 50 mg BID-5.33-5.90-5.89-5.12-7.22-7.91-8.70-8.06-7.46-7.35-5.75-6.25-8.81-10.91-12.04-16.68-19.59-18.55-15.49-16.09-15.34-12.47-9.02-8.90
Core Period: LCI699 0.25 mg QD-0.54-1.59-2.11-2.06-4.29-4.21-4.95-5.28-3.98-3.69-2.47-5.19-6.45-7.37-10.61-11.71-13.71-14.49-13.78-13.92-14.33-13.46-7.88-3.16
Core Period: LCI699 0.5 mg BID-1.42-0.570.911.50-1.70-1.02-0.76-3.02-1.87-1.73-1.74-3.92-4.05-6.12-9.78-13.03-13.72-15.60-15.93-15.47-13.63-10.55-6.73-3.76
Core Period: LCI699 0.5 mg QD0.090.15-1.53-1.18-3.09-3.12-2.10-4.69-1.59-0.30-0.430.73-2.30-5.68-8.28-10.01-11.96-14.37-13.08-13.22-10.06-8.35-6.23-0.64
Core Period: LCI699 1.0 mg QD-4.51-3.56-4.86-4.15-3.47-5.88-5.40-5.30-4.78-3.40-4.22-4.35-7.25-9.33-11.26-12.63-15.46-14.54-12.85-12.54-12.78-7.52-5.77-3.45
Core Period: Placebo8.236.484.604.682.781.422.253.762.392.543.514.693.200.750.02-0.33-3.03-6.35-6.98-6.53-3.89-0.942.180.70

Change From Baseline in MSDBP at Week 8 LOCF

Arterial BP determinations were made after the participant was in the sitting position for 5 minutes according to the American Heart Association guidelines using a calibrated standard aneroid or mercury sphygmomanometer or a calibrated standard sphygmomanometer. The change in the MSDBP was calculated comparing the Week 8 readings to the readings taken at Baseline. The change from Baseline in MSDBP was analyzed using an ANCOVA with treatment and country as factors and Baseline MSDBP as a covariate. (NCT00817635)
Timeframe: Baseline, Week 8

InterventionmmHg (Mean)
LCI699 0.25 mg BID-4.5
LCI699 1 mg QD-6.0
LCI699 0.5 mg Followed by LCI699 1 mg BID-6.1
Eplerenone 50 mg BID-7.7
Placebo-4.8

Change From Baseline in MSSBP at Week 8 Last Observation Carried Forward (LOCF)

Arterial blood pressure (BP) determinations were made after the participant was in the sitting position for 5 minutes according to the American Heart Association guidelines using a calibrated standard aneroid or mercury sphygmomanometer or a calibrated standard sphygmomanometer. The change in the MSSBP was calculated comparing the Week 8 readings to the readings taken at Baseline. The change from Baseline in MSSBP was analyzed using an analysis of covariance model (ANCOVA) with treatment and country as factors and Baseline MSSBP as a covariate. (NCT00817635)
Timeframe: Baseline, Week 8

InterventionmmHg (Mean)
LCI699 0.25 mg BID-11.4
LCI699 1 mg QD-13.1
LCI699 0.5 mg Followed by LCI699 1 mg BID-12.5
Eplerenone 50 mg BID-18.7
Placebo-8.8

Dose/Exposure BP Response Relationship of LCI699, as Measured by Change From Baseline in MSDBP at Week 8

Arterial BP determinations were made after the participant was in the sitting position for 5 minutes according to the American Heart Association guidelines using a calibrated standard aneroid or mercury sphygmomanometer or a calibrated standard sphygmomanometer. The change in the MSDBP was calculated comparing the Week 8 readings to the readings taken at Baseline. The change from Baseline in MSDBP was analyzed using an ANCOVA with treatment and country as factors and Baseline MSDBP as a covariate. (NCT00817635)
Timeframe: Baseline, Week 8

InterventionmmHg (Mean)
LCI699 0.25 mg BID-4.5
LCI699 1 mg QD-6.0
LCI699 0.5 mg Followed by LCI699 1 mg BID-6.1

Dose/Exposure BP Response Relationship of LCI699, as Measured by Change From Baseline in MSSBP at Week 8

Arterial BP determinations were made after the participant was in the sitting position for 5 minutes according to the American Heart Association guidelines using a calibrated standard aneroid or mercury sphygmomanometer or a calibrated standard sphygmomanometer. The change in the MSSBP was calculated comparing the Week 8 readings to the readings taken at Baseline. The change from Baseline in MSSBP was analyzed using an ANCOVA with treatment and country as factors and Baseline MSSBP as a covariate. (NCT00817635)
Timeframe: Baseline, Week 8

InterventionmmHg (Mean)
LCI699 0.25 mg BID-11.4
LCI699 1 mg QD-13.1
LCI699 0.5 mg Followed by LCI699 1 mg BID-12.5

Number of Participants With Cortisol Levels Below 500 Nmol/L at 1 Hour After Adrenocorticotropic Hormone (ACTH) Injection at Week 8

Serum cortisol concentrations at 1 hour after injection were measured to assess the maximum stimulated cortisol level achieved. Potential adrenal suppression was indicated if the serum cortisol concentration was <500 nanomoles per liter (nmol/L) at 1 hour after the injection. (NCT00817635)
Timeframe: 1-hour post-dose at Week 8

InterventionParticipants (Count of Participants)
LCI699 0.25 mg BID0
LCI699 1 mg QD1
LCI699 0.5 mg Followed by LCI699 1 mg BID4
Eplerenone 50 mg BID0
Placebo0

Percent Change From Baseline in RAAS Biomarker: Active Renin (ARC) in LCI699 Compared to Eplerenone 50mg at Week 8 LOCF

Percent change from Baseline was analyzed by ANCOVA model using active renin values measured at Baseline and Week 8 LOCF, with treatment and country as factors and Baseline value as the covariate. Negative percent change from Baseline shows improvement. (NCT00817635)
Timeframe: Baseline, Week 8

Interventionpercent change in ARC (Geometric Least Squares Mean)
LCI699 0.25 mg BID73.1
LCI699 1 mg QD72.8
LCI699 0.5 mg Followed by LCI699 1 mg BID156.4
Eplerenone 50 mg BID430.6

Percent Change From Baseline in RAAS Biomarker: Plasma Renin Activity (PRA) in LCI699 Compared to Eplerenone 50mg at Week 8 LOCF

Percent change from Baseline was analyzed by ANCOVA model using plasma renin values measured at Baseline and Week 8 LOCF, with treatment and country as factors and Baseline value as the covariate. Negative percent change from Baseline shows improvement. (NCT00817635)
Timeframe: Baseline, Week 8

Interventionpercent change in PRA (Geometric Least Squares Mean)
LCI699 0.25 mg BID41.6
LCI699 1 mg QD74.3
LCI699 0.5 mg Followed by LCI699 1 mg BID107.7
Eplerenone 50 mg BID414.1

Percent Change From Baseline in RAAS Biomarker: Ratio of PA to PRA in LCI699 Compared to Eplerenone 50mg at Week 8 LOCF

Percent change from Baseline was analyzed by ANCOVA model using percent ratio of PA to PRA values measured at Baseline and Week 8 LOCF, with treatment and country as factors and Baseline value as the covariate. Negative percent change from Baseline shows improvement. (NCT00817635)
Timeframe: Baseline, Week 8

Interventionpercent change in ratio of PA to PRA (Geometric Least Squares Mean)
LCI699 0.25 mg BID-46.7
LCI699 1 mg QD-50.0
LCI699 0.5 mg Followed by LCI699 1 mg BID-78.3
Eplerenone 50 mg BID-57.1

Percent Change From Baseline in Renin-Angiotensin-Aldosterone-System (RAAS) Biomarker: Plasma Aldosterone (PA) in LCI699 Compared to Eplerenone 50 mg at Week 8 LOCF

Percent change from Baseline was analyzed by ANCOVA model using PA values measured at Baseline and Week 8 LOCF, with treatment and country as factors and Baseline value as the covariate. Negative percent change from Baseline shows improvement. (NCT00817635)
Timeframe: Baseline, Week 8

Interventionpercent change in aldosterone (Geometric Least Squares Mean)
LCI699 0.25 mg BID-22.3
LCI699 1 mg QD-30.4
LCI699 0.5 mg Followed by LCI699 1 mg BID-53.1
Eplerenone 50 mg BID115.0

Change From Baseline in Mean 24 Hours, Mean Daytime and Mean Nighttime DBP in LCI699 1mg QD Versus LCI699 0.5mg BID Arm at Week 4, as Measured by ABPM

An ABPM measured a participant's blood pressure over a 24-hour period including daytime and nighttime readings using an automated validated monitoring device from Baseline to Week 4. The 24-hour DBP was calculated by taking the mean of all ambulatory diastolic blood pressure readings for the 24-hour period. The change from Baseline in DBP was analyzed using an ANCOVA with treatment and country as factors and Baseline MSDBP as a covariate. (NCT00817635)
Timeframe: Baseline, Week 4

,
InterventionmmHg (Mean)
24-hour Mean DBPDaytime Mean DBPNighttime Mean DBP
LCI699 0.5 mg BID-2.5-2.6-2.8
LCI699 1 mg QD-4.3-3.9-4.5

Change From Baseline in Mean 24 Hours, Mean Daytime and Mean Nighttime Diastolic Blood Pressure (DBP) at Week 8 LOCF, as Measured by ABPM

An ABPM measured a participant's blood pressure over a 24-hour period including daytime and nighttime readings, using an automated validated monitoring device from Baseline to Week 8. The 24-hour DBP was calculated by taking the mean of all ambulatory diastolic blood pressure readings for the 24-hour period. The change from Baseline in DBP was analyzed using an ANCOVA with treatment and country as factors and Baseline MSDBP as a covariate. (NCT00817635)
Timeframe: Baseline, Week 8

,,,,
InterventionmmHg (Mean)
24-hour Mean DBPDaytime Mean DBPNighttime Mean DBP
Eplerenone 50 mg BID-9.6-9.5-9.6
LCI699 0.25 mg BID1.00.61.9
LCI699 0.5 mg Followed by LCI699 1 mg BID-3.7-3.4-4.6
LCI699 1 mg QD-3.4-3.6-2.5
Placebo-0.2-0.81.2

Change From Baseline in Mean 24 Hours, Mean Daytime and Mean Nighttime SBP in LCI699 1mg QD Versus LCI699 0.5mg BID Arm at Week 4, as Measured by ABPM

An ABPM measured a participant's blood pressure over a 24-hour period including daytime and nighttime readings using an automated validated monitoring device from Baseline to Week 4. The 24-hour SBP was calculated by taking the mean of all ambulatory systolic blood pressure readings for the 24-hour period. The change from Baseline in SBP was analyzed using an ANCOVA with treatment and country as factors and Baseline MSDBP as a covariate. (NCT00817635)
Timeframe: Baseline, Week 4

,
InterventionmmHg (Mean)
24-hour Mean SBPDaytime Mean SBPNighttime Mean SBP
LCI699 0.5 mg BID-4.7-5.3-4.5
LCI699 1 mg QD-7.8-8.1-6.8

Change From Baseline in Mean 24 Hours, Mean Daytime and Mean Nighttime Systolic Blood Pressure (SBP) at Week 8 LOCF, as Measured by Ambulatory Blood Pressure Measurement (ABPM)

An ABPM measured a participant's blood pressure over a 24-hour period including daytime and nighttime readings, using an automated validated monitoring device from Baseline to Week 8. The 24-hour SBP was calculated by taking the mean of all ambulatory systolic blood pressure readings for the 24-hour period. The change from Baseline in SBP was analyzed using ANCOVA with treatment and country as factors and Baseline MSSBP as a covariate. (NCT00817635)
Timeframe: Baseline, Week 8

,,,,
InterventionmmHg (Mean)
24-hour Mean SBPDaytime Mean SBPNighttime Mean SBP
Eplerenone 50 mg BID-15.7-15.7-15.4
LCI699 0.25 mg BID-4.4-4.9-3.2
LCI699 0.5 mg Followed by LCI699 1 mg BID-6.3-6.3-7.0
LCI699 1 mg QD-5.7-6.0-4.8
Placebo-1.0-1.60.4

Number of Participants With Adverse Event (AEs), Serious Adverse Events (SAEs), Hyperkalemia, and Hyponatremia

An AE was an adverse medical event which occurs in a participant of the study and which is not necessarily in a causal relationship with the treatment the participant receives. SAEs were AEs leading to death, are life-threatening, require hospitalizations or prolongation of hospitalizations, represent an innate malformation or a congenital abnormality. Hyperkalemia was defined as potassium level >5.5 millimoles per liter (mmol/L). It is the medical term that describes a potassium level that's higher than normal. Hyponatremia was defined as sodium level <135 mmol/L. It is the medical term that describes a sodium level that's lesser than normal. (NCT00817635)
Timeframe: AEs, Hyperkalemia, and Hyponatremia: From start of the study drug treatment up to 10 weeks; SAE: From signing of the informed consent up to 10 weeks

,,,,
InterventionParticipants (Count of Participants)
AE(s)SAE(s)Hyperkalemia [potassium level >5.5 mmol/L]Hyperkalemia [potassium level ≥6.0 mmol/L]Hyponatremia [sodium level <130 and ≥125 mmol/L]Hyponatremia [sodium level <135 mmol/L and ≥130mmol/L]
Eplerenone 50 mg BID1310013
LCI699 0.25 mg BID1502203
LCI699 0.5 mg Followed by LCI699 1 mg BID800007
LCI699 1 mg QD1500002
Placebo1601002

Percentage of Participants With a MSDBP Response and MSDBP Control at Week 8, as Measured by OBP

MSDBP response was defined as the percentage of participants with a MSDBP <90 mmHg or a >=10 mmHg reduction from baseline. MSDBP control was defined as the percentage of participants with a MSDBP <90 mmHg for non-diabetic participants and <80mHg for diabetic participants. (NCT00817635)
Timeframe: Week 8

,,,,
Interventionpercentage of participants (Number)
MSDBP ResponseMSDBP Control
Eplerenone 50 mg BID71.956.3
LCI699 0.25 mg BID67.754.8
LCI699 0.5 mg Followed by LCI699 1 mg BID71.058.1
LCI699 1 mg QD73.165.4
Placebo57.654.5

Percentage of Participants With a MSSBP Response and MSSBP Control at Week 8, as Measured by Office Blood Pressure (OBP)

MSSBP response was defined as the percentage of participants with a MSSBP <140 mmHg or a >=20 mmHg reduction from baseline reduction from baseline. MSSBP control was defined as the percentage of participants with a MSSBP <140 mmHg for non-diabetic participants and <130mHg for diabetic participants. (NCT00817635)
Timeframe: Week 8

,,,,
Interventionpercentage of participants (Number)
MSSBP ResponseMSSBP Control
Eplerenone 50 mg BID65.653.1
LCI699 0.25 mg BID54.851.6
LCI699 0.5 mg Followed by LCI699 1 mg BID41.932.3
LCI699 1 mg QD57.750.0
Placebo42.436.4

Reviews

7 reviews available for aldosterone and Hypertension, Essential

ArticleYear
The Effect of Aldosterone on Cardiorenal and Metabolic Systems.
    International journal of molecular sciences, 2023, Mar-11, Volume: 24, Issue:6

    Topics: Aldosterone; Cardiovascular Diseases; Essential Hypertension; Humans; Hyperaldosteronism; Hypertensi

2023
Primary aldosteronism is a public health issue: challenges and opportunities.
    Journal of human hypertension, 2020, Volume: 34, Issue:7

    Topics: Aldosterone; Blood Pressure; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension; Publi

2020
Excessive Catecholamine Secretion and the Activation of the Renin-Angiotensin-Aldosterone-System in Patients with Pheochromocytoma: A Single Center Experience and Overview of the Literature.
    Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 2017, Volume: 49, Issue:10

    Topics: Adrenal Gland Neoplasms; Aldosterone; Catecholamines; Essential Hypertension; Female; Humans; Male;

2017
Aldosterone and Left Ventricular Remodeling.
    Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 2015, Volume: 47, Issue:13

    Topics: Aldosterone; Essential Hypertension; Heart Ventricles; Humans; Hyperaldosteronism; Hypertension; Ven

2015
MECHANISMS IN ESSENTIAL HYPERTENSION.
    Diseases of the chest, 1964, Volume: 45

    Topics: Aldosterone; Angiotensins; Catecholamines; Essential Hypertension; Guanethidine; Hypertension; Miner

1964
[METABOLIC DATA ON HYPERTENSION (ESSENTIAL HYPERTENSION)].
    Lekarska veda v zahranici, 1964, Aug-21, Volume: 22

    Topics: Adrenal Glands; Aldosterone; Angiotensins; Arteriosclerosis; Autonomic Nervous System Diseases; Cate

1964
[NEW DATA ON THE ETIOPATHOGENESIS OF ESSENTIAL ARTERIAL HYPERTENSION].
    Studii si cercetari de medicina interna, 1965, Volume: 40

    Topics: Aldosterone; Electrolytes; Essential Hypertension; Humans; Hypertension; Metabolism

1965

Trials

4 trials available for aldosterone and Hypertension, Essential

ArticleYear
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
    Journal of hypertension, 2013, Volume: 31, Issue:10

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Aldosterone; Antihypertensive Agents; Biomarkers; Blood Pre

2013
Marinobufagenin in essential hypertension and primary aldosteronism: a cardiotonic steroid with clinical and diagnostic implications.
    Clinical and experimental hypertension (New York, N.Y. : 1993), 2015, Volume: 37, Issue:2

    Topics: Aldosterone; Blood Pressure; Bufanolides; Carotid Intima-Media Thickness; Essential Hypertension; Fe

2015
TET2 and CSMD1 genes affect SBP response to hydrochlorothiazide in never-treated essential hypertensives.
    Journal of hypertension, 2015, Volume: 33, Issue:6

    Topics: Adult; Aged; Aldosterone; Antihypertensive Agents; Blood Pressure; Case-Control Studies; Dioxygenase

2015
Changeover Trial of Azilsartan and Olmesartan Comparing Effects on the Renin-Angiotensin-Aldosterone System in Patients with Essential Hypertension after Cardiac Surgery (CHAOS Study).
    Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia, 2016, Jun-20, Volume: 22, Issue:3

    Topics: Aged; Aldosterone; Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Antihypertensive Agents;

2016

Other Studies

85 other studies available for aldosterone and Hypertension, Essential

ArticleYear
Modulation of 11β-hydroxysteroid dehydrogenase functions by the cloud of endogenous metabolites in a local microenvironment: The glycyrrhetinic acid-like factor (GALF) hypothesis.
    The Journal of steroid biochemistry and molecular biology, 2021, Volume: 214

    Topics: 11-beta-Hydroxysteroid Dehydrogenases; Aldosterone; Animals; Blood Pressure; Corticosterone; Essenti

2021
Evaluation of Intra-Renal Stiffness in Patients with Primary Aldosteronism.
    High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension, 2022, Volume: 29, Issue:1

    Topics: Adult; Aged; Aldosterone; Essential Hypertension; Female; Humans; Hyperaldosteronism; Hypertension;

2022
A pilot study to evaluate the erythrocyte glycocalyx sensitivity to sodium as a marker for cellular salt sensitivity in hypertension.
    Journal of human hypertension, 2023, Volume: 37, Issue:4

    Topics: Aldosterone; Blood Pressure; Erythrocytes; Essential Hypertension; Female; Glycocalyx; Humans; Hyper

2023
Radiomics utilization to differentiate nonfunctional adenoma in essential hypertension and functional adenoma in primary aldosteronism.
    Scientific reports, 2022, 05-25, Volume: 12, Issue:1

    Topics: Adenoma; Adrenalectomy; Aldosterone; Essential Hypertension; Humans; Hyperaldosteronism; Retrospecti

2022
Divergent Characteristics of T-Cell Receptor Repertoire Between Essential Hypertension and Aldosterone-Producing Adenoma.
    Frontiers in immunology, 2022, Volume: 13

    Topics: Adenoma; Aldosterone; Essential Hypertension; Humans; Hypertension; Receptors, Antigen, T-Cell; Reni

2022
Association between Vitamin D Deficiency and Levels of Renin and Angiotensin in Essential Hypertension.
    International journal of clinical practice, 2022, Volume: 2022

    Topics: Adult; Aldosterone; Angiotensins; Asian People; Blood Pressure; Essential Hypertension; Female; Huma

2022
Circulating Plasma Concentrations of ACE2 in Primary Aldosteronism and Cardiovascular Outcomes.
    The Journal of clinical endocrinology and metabolism, 2022, 11-25, Volume: 107, Issue:12

    Topics: Adrenalectomy; Aldosterone; Angiotensin-Converting Enzyme 2; Cardiovascular Diseases; Essential Hype

2022
Serum aldosterone effect on left ventricular structure and diastolic function in essential hypertension.
    Journal of clinical hypertension (Greenwich, Conn.), 2023, Volume: 25, Issue:2

    Topics: Aldosterone; Diastole; Echocardiography; Essential Hypertension; Female; Humans; Hypertension; Hyper

2023
Aldosterone Synthase Inhibitors and the Treatment of Essential Hypertension.
    The Journal of clinical endocrinology and metabolism, 2023, Jul-14, Volume: 108, Issue:8

    Topics: Aldosterone; Cytochrome P-450 CYP11B2; Essential Hypertension; Humans; Hyperaldosteronism; Hypertens

2023
KCNJ5 mutation is a predictor for recovery of endothelial function after adrenalectomy in patients with aldosterone-producing adenoma.
    Hypertension research : official journal of the Japanese Society of Hypertension, 2023, Volume: 46, Issue:9

    Topics: Adenoma; Adrenalectomy; Aldosterone; Ankle Brachial Index; Essential Hypertension; G Protein-Coupled

2023
Central diastolic blood pressure, plasma aldosterone and uric acid are associated with microalbuminuria in essential hypertension: a case-control study.
    BMC cardiovascular disorders, 2023, 10-17, Volume: 23, Issue:1

    Topics: Albuminuria; Aldosterone; Blood Pressure; Case-Control Studies; Essential Hypertension; Humans; Hype

2023
Renin-Angiotensin-Aldosterone System Triple-A Analysis for the Screening of Primary Aldosteronism.
    Hypertension (Dallas, Tex. : 1979), 2020, Volume: 75, Issue:1

    Topics: Adult; Aldosterone; Angiotensin I; Angiotensin II; Essential Hypertension; Female; Humans; Hyperaldo

2020
The relationship of plasma renin, angiotensin, and aldosterone levels to blood pressure variability and target organ damage in children with essential hypertension.
    BMC cardiovascular disorders, 2020, 06-16, Volume: 20, Issue:1

    Topics: Adolescent; Age Factors; Aldosterone; Angiotensins; Biomarkers; Blood Pressure; Child; Essential Hyp

2020
Associations Between Metabolic Profiles and Target-Organ Damage in Chinese Individuals With Primary Aldosteronism.
    Frontiers in endocrinology, 2020, Volume: 11

    Topics: Adult; Aldosterone; Asian People; Case-Control Studies; China; Essential Hypertension; Female; Human

2020
Confirmatory testing of primary aldosteronism with saline infusion test and LC-MS/MS.
    European journal of endocrinology, 2021, Volume: 184, Issue:1

    Topics: Adult; Aged; Aldosterone; Blood Chemical Analysis; Chromatography, Liquid; Cohort Studies; Diagnosis

2021
Correlation between serum microRNA-136 levels and RAAS biochemical markers in patients with essential hypertension.
    European review for medical and pharmacological sciences, 2020, Volume: 24, Issue:22

    Topics: Adult; Aged; Aldosterone; Biomarkers; Essential Hypertension; Female; Humans; Male; MicroRNAs; Middl

2020
Growth differentiation factor 15 levels are similar in primary aldosteronism and essential hypertension and do not predict arterial inflammation.
    Journal of hypertension, 2021, 03-01, Volume: 39, Issue:3

    Topics: Aldosterone; Arteritis; Essential Hypertension; Growth Differentiation Factor 15; Humans; Hyperaldos

2021
Novel chemiluminescent immunoassay to measure plasma aldosterone and plasma active renin concentrations for the diagnosis of primary aldosteronism.
    Journal of human hypertension, 2022, Volume: 36, Issue:1

    Topics: Aldosterone; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension; Radioimmunoassay; Ren

2022
Hemodynamic and Non-Hemodynamic Components of Cardiac Remodeling in Primary Aldosteronism.
    Frontiers in endocrinology, 2021, Volume: 12

    Topics: Adrenalectomy; Adrenocortical Adenoma; Adult; Aldosterone; Blood Pressure; Echocardiography; Essenti

2021
Aldosterone hyperreactivity to acute psychosocial stress induction in men with essential hypertension.
    Hormones and behavior, 2021, Volume: 134

    Topics: Aldosterone; Blood Pressure; Essential Hypertension; Humans; Hypertension; Male; Stress, Psychologic

2021
Evaluation of Abdominal Computed Tomography Scans for Differentiating the Discrepancies in Abdominal Adipose Tissue Between Two Major Subtypes of Primary Aldosteronism.
    Frontiers in endocrinology, 2021, Volume: 12

    Topics: Abdominal Fat; Adult; Aged; Aldosterone; Databases, Factual; Essential Hypertension; Female; Humans;

2021
Lipid Profiles in Primary Aldosteronism Compared with Essential Hypertension: Propensity-Score Matching Study.
    Endocrinology and metabolism (Seoul, Korea), 2021, Volume: 36, Issue:4

    Topics: Aldosterone; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension; Lipids; Retrospective

2021
Aldosterone a Relevant Factor in the Beginning and Evolution of Arterial Hypertension.
    American journal of hypertension, 2017, 05-01, Volume: 30, Issue:5

    Topics: Aldosterone; Essential Hypertension; Humans; Hypertension; Renin

2017
Plasma renin activity to plasma aldosterone concentration ratio correlates with night-time and pulse pressures in essential hypertensive patients treated with angiotensin-converting enzyme inhibitors/AT1 blockers.
    Journal of hypertension, 2017, Volume: 35, Issue:11

    Topics: Aldosterone; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Biom

2017
Aldosterone induces left ventricular subclinical systolic dysfunction: a strain imaging study.
    Journal of hypertension, 2018, Volume: 36, Issue:2

    Topics: Adult; Aged; Aldosterone; Echocardiography; Essential Hypertension; Female; Heart; Humans; Hyperaldo

2018
Inflammation and Fibrosis in Perirenal Adipose Tissue of Patients With Aldosterone-Producing Adenoma.
    Endocrinology, 2018, 01-01, Volume: 159, Issue:1

    Topics: 3T3-L1 Cells; Adenoma; Adipocytes, Brown; Adipogenesis; Adipokines; Adrenalectomy; Aldosterone; Anim

2018
Confirmatory Tests for the Diagnosis of Primary Aldosteronism: A Prospective Diagnostic Accuracy Study.
    Hypertension (Dallas, Tex. : 1979), 2018, Volume: 71, Issue:1

    Topics: Adrenal Cortex; Adrenal Cortex Function Tests; Adult; Aldosterone; Captopril; Clinical Chemistry Tes

2018
Evaluation of the Saline Infusion Test and the Captopril Challenge Test in Chinese Patients With Primary Aldosteronism.
    The Journal of clinical endocrinology and metabolism, 2018, 03-01, Volume: 103, Issue:3

    Topics: Adrenal Cortex Function Tests; Adult; Aldosterone; Asian People; Captopril; Essential Hypertension;

2018
IL-6 trans-signalling contributes to aldosterone-induced cardiac fibrosis.
    Cardiovascular research, 2018, 04-01, Volume: 114, Issue:5

    Topics: Adult; Aldosterone; Animals; Cardiomegaly; Case-Control Studies; Cells, Cultured; Collagen; Cytokine

2018
Criteria for diagnosing primary aldosteronism on the basis of liquid chromatography-tandem mass spectrometry determinations of plasma aldosterone concentration.
    Journal of hypertension, 2018, Volume: 36, Issue:7

    Topics: Adolescent; Adult; Aged; Aldosterone; Case-Control Studies; Chromatography, Liquid; Essential Hypert

2018
Untangling Essential Hypertension: The Potential Roles of Aldosterone and Atrial Natriuretic Peptide.
    Mayo Clinic proceedings, 2018, Volume: 93, Issue:8

    Topics: Aldosterone; Antihypertensive Agents; Atrial Natriuretic Factor; Essential Hypertension; Humans; Hyp

2018
Obesity as a Key Factor Underlying Idiopathic Hyperaldosteronism.
    The Journal of clinical endocrinology and metabolism, 2018, 12-01, Volume: 103, Issue:12

    Topics: Adult; Aldosterone; Cross-Sectional Studies; Diabetes Mellitus; Dyslipidemias; Essential Hypertensio

2018
Microvascular endothelial function is impaired in patients with idiopathic hyperaldosteronism.
    Hypertension research : official journal of the Japanese Society of Hypertension, 2018, Volume: 41, Issue:11

    Topics: Adult; Aldosterone; Blood Pressure; Endothelium, Vascular; Essential Hypertension; Female; Humans; H

2018
PTH Modulation by Aldosterone and Angiotensin II is Blunted in Hyperaldosteronism and Rescued by Adrenalectomy.
    The Journal of clinical endocrinology and metabolism, 2019, 09-01, Volume: 104, Issue:9

    Topics: Adenoma; Adrenal Hyperplasia, Congenital; Adrenalectomy; Aldosterone; Angiotensin II; Antihypertensi

2019
Subclinical atherosclerosis due to increase of plasma aldosterone concentrations in essential hypertensive individuals.
    Journal of hypertension, 2019, Volume: 37, Issue:11

    Topics: Adult; Aldosterone; Ankle Brachial Index; Atherosclerosis; Biomarkers; Carotid Intima-Media Thicknes

2019
Aldosterone Induces Vascular Damage.
    Hypertension (Dallas, Tex. : 1979), 2019, Volume: 74, Issue:3

    Topics: Adult; Aldosterone; Antihypertensive Agents; Area Under Curve; Arterial Pressure; Cohort Studies; Cr

2019
Urinary sodium excretion is the main determinant of mineralocorticoid excretion rates in patients with chronic kidney disease.
    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2013, Volume: 28, Issue:6

    Topics: Aldosterone; Cohort Studies; Corticosterone; Cross-Sectional Studies; Essential Hypertension; Female

2013
Aldosterone levels and inflammatory stimulation in essential hypertensive patients.
    Journal of human hypertension, 2013, Volume: 27, Issue:9

    Topics: Adult; Aged; Aldosterone; Biomarkers; Blood Pressure; C-Reactive Protein; Cardiovascular Diseases; C

2013
Serum dehydroepiandrosterone sulfate concentration is lower in women with primary aldosteronism.
    Journal of the renin-angiotensin-aldosterone system : JRAAS, 2015, Volume: 16, Issue:1

    Topics: Adenoma; Adult; Aged; Aldosterone; Cholesterol, HDL; Creatinine; Dehydroepiandrosterone Sulfate; Ess

2015
Bone health and aldosterone excess.
    Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 2013, Volume: 24, Issue:11

    Topics: Absorptiometry, Photon; Adult; Aged; Aldosterone; Bone Density; Calcium; Essential Hypertension; Fem

2013
Comparison of 24-h urinary aldosterone level and random urinary aldosterone-to-creatinine ratio in the diagnosis of primary aldosteronism.
    PloS one, 2013, Volume: 8, Issue:6

    Topics: Adenoma; Adrenal Gland Neoplasms; Adult; Aldosterone; Creatinine; Essential Hypertension; Female; Hu

2013
Quantification of urinary 18-hydroxycortisol using LC-MS/MS.
    Annals of clinical biochemistry, 2013, Volume: 50, Issue:Pt 5

    Topics: Adenoma; Adrenal Gland Neoplasms; Aldosterone; Biomarkers, Tumor; Chromatography, Liquid; Essential

2013
[Analysis of characteristics of renin, aldosterone and aldosterone/renin ratio in patients with aldosterone-producing adenoma].
    Zhonghua yi xue za zhi, 2013, Nov-12, Volume: 93, Issue:42

    Topics: Adrenal Gland Neoplasms; Adult; Aldosterone; Case-Control Studies; Essential Hypertension; Female; H

2013
Measurement of plasma renin concentration instead of plasma renin activity decreases the positive aldosterone-to-renin ratio tests in treated patients with essential hypertension.
    Journal of hypertension, 2014, Volume: 32, Issue:3

    Topics: Adolescent; Adult; Aged; Aged, 80 and over; Aldosterone; Antihypertensive Agents; Blood Chemical Ana

2014
[Influence factors of salt-sensitive hypertension and responses of blood pressure and urinary sodium and potassium excretion to acute oral saline loading among essential hypertensive patients].
    Zhonghua xin xue guan bing za zhi, 2013, Volume: 41, Issue:12

    Topics: Adult; Aged; Aldosterone; Blood Pressure; Electrolytes; Essential Hypertension; Female; Humans; Hype

2013
Aldosterone to active Renin ratio as screening test for primary aldosteronism: reproducibility and influence of orthostasis and salt loading.
    Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 2014, Volume: 46, Issue:6

    Topics: Aldosterone; Cohort Studies; Dizziness; Essential Hypertension; Female; Humans; Hyperaldosteronism;

2014
Primary aldosteronism and essential hypertension: assessment of cardiovascular risk at diagnosis and after treatment.
    Nutrition, metabolism, and cardiovascular diseases : NMCD, 2014, Volume: 24, Issue:5

    Topics: Adult; Aged; Aldosterone; Blood Glucose; Blood Pressure; Cardiovascular Diseases; Essential Hyperten

2014
Association between urine aldosterone and diastolic function in patients with primary aldosteronism and essential hypertension.
    Clinical biochemistry, 2014, Volume: 47, Issue:13-14

    Topics: Adult; Aldosterone; Echocardiography; Essential Hypertension; Female; Humans; Hyperaldosteronism; Hy

2014
Oxidative stress in patients affected by primary aldosteronism.
    Journal of hypertension, 2014, Volume: 32, Issue:10

    Topics: Adenoma; Adrenalectomy; Adult; Aged; Aldosterone; Essential Hypertension; Female; Humans; Hyperaldos

2014
Decreased plasma prorenin levels in primary aldosteronism: potential diagnostic implications.
    Journal of hypertension, 2015, Volume: 33, Issue:1

    Topics: Adenoma; Adult; Aldosterone; Cohort Studies; Essential Hypertension; Female; Humans; Hyperaldosteron

2015
Plasma aldosterone and left ventricular diastolic function in treatment-naïve patients with hypertension: tissue-Doppler imaging study.
    Hypertension (Dallas, Tex. : 1979), 2015, Volume: 65, Issue:6

    Topics: Adult; Aldosterone; Analysis of Variance; Case-Control Studies; Chi-Square Distribution; Diastole; E

2015
Stress-induced Aldosterone Hyper-Secretion in a Substantial Subset of Patients With Essential Hypertension.
    The Journal of clinical endocrinology and metabolism, 2015, Volume: 100, Issue:8

    Topics: Adenoma; Adrenal Gland Neoplasms; Adrenocorticotropic Hormone; Aldosterone; Case-Control Studies; Cy

2015
[The inversion of concepts about biological role of system rennin-angiotensin II- aldosterone and functions of arterial tension as a metabolism regulator].
    Klinicheskaia laboratornaia diagnostika, 2015, Volume: 60, Issue:2

    Topics: Aldosterone; Angiotensin II; Arterial Pressure; Arteries; Chymosin; Essential Hypertension; Humans;

2015
Obstructive Sleep Apnea Using Watch-PAT 200 Is Independently Associated With an Increase in Morning Blood Pressure Surge in Never-Treated Hypertensive Patients.
    Journal of clinical hypertension (Greenwich, Conn.), 2015, Volume: 17, Issue:9

    Topics: Adult; Aldosterone; Blood Pressure; Blood Pressure Determination; Blood Pressure Monitoring, Ambulat

2015
Prevalence of Liddle Syndrome Among Young Hypertension Patients of Undetermined Cause in a Chinese Population.
    Journal of clinical hypertension (Greenwich, Conn.), 2015, Volume: 17, Issue:11

    Topics: Adult; Aldosterone; China; Diagnostic Errors; Essential Hypertension; Female; Humans; Hypertension;

2015
Circulating tissue inhibitor of matrix metalloproteinase-1 is associated with aldosterone-induced diastolic dysfunction.
    Journal of hypertension, 2015, Volume: 33, Issue:9

    Topics: Adrenal Cortex Neoplasms; Adrenalectomy; Adrenocortical Adenoma; Adult; Aldosterone; Diastole; Echoc

2015
Clinical validation for the aldosterone-to-renin ratio and aldosterone suppression testing using simultaneous fully automated chemiluminescence immunoassays.
    Journal of hypertension, 2015, Volume: 33, Issue:12

    Topics: Adult; Aged; Aged, 80 and over; Aldosterone; Blood Pressure; Essential Hypertension; Female; Humans;

2015
Factors affecting parathyroid hormone levels in different types of primary aldosteronism.
    Clinical endocrinology, 2016, Volume: 85, Issue:2

    Topics: Adenoma; Adrenal Hyperplasia, Congenital; Adrenalectomy; Adult; Aldosterone; Calcium; Essential Hype

2016
[Evaluation of the ratio of plasma aldosterone to rennin concentration measured by an automated chemiluminescent immunoassay in screening for primary aldosteronism].
    Zhonghua nei ke za zhi, 2016, Volume: 55, Issue:1

    Topics: Aldosterone; Area Under Curve; Case-Control Studies; Chymosin; Essential Hypertension; Humans; Hyper

2016
[An evaluation of plasma aldosterone-to-active-renin ratio in different postures in combination with aldosterone concentration in the diagnosis of aldosteronoma].
    Zhonghua nei ke za zhi, 2016, Volume: 55, Issue:6

    Topics: Aldosterone; Asian People; China; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension;

2016
Aldosterone-Renin Ratio and Side-Selective Renal Perfusion in Essential Hypertension.
    American journal of hypertension, 2016, 11-01, Volume: 29, Issue:11

    Topics: Aldosterone; Blood Pressure; Essential Hypertension; Humans; Hypertension; Kidney; Renin; Renin-Angi

2016
Endogenous ouabain and aldosterone are coelevated in the circulation of patients with essential hypertension.
    Journal of hypertension, 2016, Volume: 34, Issue:10

    Topics: Adult; Aldosterone; Blood Pressure; Essential Hypertension; Female; Humans; Hyperaldosteronism; Hype

2016
Cortisol/cortisone ratio and matrix metalloproteinase-9 activity are associated with pediatric primary hypertension.
    Journal of hypertension, 2016, Volume: 34, Issue:9

    Topics: Adiponectin; Adolescent; Aldosterone; Blood Pressure; Body Mass Index; C-Reactive Protein; Child; Ch

2016
Cholecalciferol treatment downregulates renin-angiotensin system and improves endothelial function in essential hypertensive patients with hypovitaminosid D.
    Journal of hypertension, 2016, Volume: 34, Issue:11

    Topics: Adult; Aldosterone; Angiotensin II; Blood Pressure; Cardiovascular Diseases; Cholecalciferol; Endoth

2016
Increased urinary excretion of the epithelial Na channel activator prostasin in patients with primary aldosteronism.
    Journal of hypertension, 2017, Volume: 35, Issue:2

    Topics: Adult; Aldosterone; Biomarkers; Blood Pressure; Epithelial Sodium Channels; Essential Hypertension;

2017
Role of adrenocorticotropic hormone in essential hypertension and primary aldosteronism.
    Journal of clinical hypertension (Greenwich, Conn.), 2017, Volume: 19, Issue:3

    Topics: Adenoma; Adrenocorticotropic Hormone; Aldosterone; Blood Pressure; Essential Hypertension; Humans; H

2017
Plasma adrenocorticotropic hormone but not aldosterone is correlated with blood pressure in patients with aldosterone-producing adenomas.
    Journal of clinical hypertension (Greenwich, Conn.), 2017, Volume: 19, Issue:3

    Topics: Adenoma; Adrenocorticotropic Hormone; Adult; Aged; Aldosterone; Blood Pressure; Essential Hypertensi

2017
Plasma aldosterone level within the normal range is less associated with cardiovascular and cerebrovascular risk in primary aldosteronism.
    Journal of hypertension, 2017, Volume: 35, Issue:5

    Topics: Adult; Aged; Aldosterone; Blood Pressure; Cardiovascular Diseases; Cross-Sectional Studies; Essentia

2017
Plasma and urinary metanephrines determined by an enzyme immunoassay, but not serum chromogranin A for the diagnosis of pheochromocytoma in patients with adrenal mass.
    Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association, 2012, Volume: 120, Issue:8

    Topics: Adrenal Gland Neoplasms; Adrenocortical Adenoma; Adult; Aldosterone; Chromogranin A; Diagnosis, Diff

2012
Association of elevated plasma aldosterone-to-renin ratio with future cardiovascular events in patients with essential hypertension.
    Journal of hypertension, 2012, Volume: 30, Issue:12

    Topics: Adult; Aged; Aldosterone; Asian People; Cardiovascular Diseases; Cohort Studies; Essential Hypertens

2012
Cholecalciferol administration blunts the systemic renin-angiotensin system in essential hypertensives with hypovitaminosis D.
    Journal of the renin-angiotensin-aldosterone system : JRAAS, 2014, Volume: 15, Issue:1

    Topics: Adult; Aged; Aldosterone; Angiotensin II; Cholecalciferol; Essential Hypertension; Female; Humans; H

2014
Aldosteronism and hypertension: the influence of complete adrenalectomy upon essential hypertension in a child.
    Pediatrics, 1959, Volume: 23, Issue:6

    Topics: Adrenalectomy; Aldosterone; Child; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension;

1959
Aldosterone excretion in essential hypertension.
    The Journal of clinical endocrinology and metabolism, 1960, Volume: 20

    Topics: Aldosterone; Biological Transport; Body Fluids; Essential Hypertension; Humans; Hypertension

1960
[Urinary excretion of aldosterone in essential hypertension. Investigations by a chemical method].
    Folia endocrinologica; mensile di incretologia e incretoterapia, 1960, Volume: 13

    Topics: Aldosterone; Body Fluids; Essential Hypertension; Humans; Hypertension

1960
[Conn's syndrome and essential arterial hypertension].
    Il Progresso medico, 1960, Aug-15, Volume: 16

    Topics: Aldosterone; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension

1960
Essential hypertension and aldosterone.
    Circulation, 1961, Volume: 23

    Topics: Aldosterone; Essential Hypertension; Humans; Hypertension

1961
[Natruresis and aldosterone excretion in essential hypertension].
    Schweizerische medizinische Wochenschrift, 1959, Apr-04, Volume: 89

    Topics: Aldosterone; Biological Transport; Body Fluids; Essential Hypertension; Humans; Hypertension; Sodium

1959
Surgical treatment of hypertension -- primary aldosteronism. A review of 13 cases.
    The New England journal of medicine, 1962, 01-25, Volume: 266

    Topics: Adrenal Cortex; Adrenal Cortex Neoplasms; Aldosterone; Essential Hypertension; Humans; Hyperaldoster

1962
Effect of chlorothiazide upon aldosterone excretion and sodium and potassium balance in essential hypertension.
    The Journal of laboratory and clinical medicine, 1962, Volume: 60

    Topics: Aldosterone; Body Fluids; Chlorothiazide; Essential Hypertension; Humans; Hypertension; Potassium; S

1962
Influence of alterations in sodium intake on urinary aldosterone response to corticotropin in normal individuals and patients with essential hypertension.
    Metabolism: clinical and experimental, 1962, Volume: 11

    Topics: Adrenocorticotropic Hormone; Aldosterone; Diet; Essential Hypertension; Humans; Hypertension; Nutrit

1962
Humoral factors in essential hypertension.
    Verhandlungen der Deutschen Gesellschaft fur Kreislaufforschung, 1963, Volume: 28

    Topics: Aldosterone; Essential Hypertension; Humans; Hypertension; Renin

1963
[Intervention of aldosterone and electrolytes in the pathogenesis of essential hypertension].
    Folia endocrinologica; mensile di incretologia e incretoterapia, 1962, Volume: 15

    Topics: Aldosterone; Electrolytes; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension; Sodium;

1962
BLOOD VOLUME, TOTAL BODY WATER AND ALDOSTERONE EXCRETION IN ESSENTIAL HYPERTENSION.
    Clinical science, 1964, Volume: 26

    Topics: Aldosterone; Blood Volume; Blood Volume Determination; Body Fluids; Body Water; Chromium Isotopes; E

1964
Effects of an acute salt load in a case of primary hyperaldo-steronism before and nine months after surgical cure: comparison with normal subjects and patients with essential hypertension before and after reduction of their elevated pressure with drug tre
    The Journal of laboratory and clinical medicine, 1959, Volume: 54

    Topics: Aldosterone; Essential Hypertension; Humans; Hypertension; Sodium Chloride; Sodium Chloride, Dietary

1959
[Contribution to the treatment of essential hypertension.(Control of blood pressure, active blood volume, venous pressure, circulation time and mineral metabolism after Repicin and spirolactone medication)].
    Munchener medizinische Wochenschrift (1950), 1962, Feb-02, Volume: 104

    Topics: Aldosterone; Blood Circulation Time; Blood Pressure; Blood Pressure Determination; Blood Volume; Chl

1962