aldosterone has been researched along with Hypertension, Essential in 96 studies
Excerpt | Relevance | Reference |
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"Angiotensin II receptor blockers (ARBs) have been widely used to treat hypertension and large-scale clinical studies have shown various benefits." | 9.22 | Changeover 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)." | 8.31 | Central 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." | 7.91 | PTH 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." | 7.83 | Cortisol/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." | 7.83 | Endogenous 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)." | 7.81 | Serum 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." | 7.78 | Plasma 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." | 5.91 | Serum 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)." | 5.62 | Aldosterone 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." | 5.56 | Renin-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." | 5.48 | Inflammation 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." | 5.48 | Criteria 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." | 5.46 | Plasma 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." | 5.42 | Plasma 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." | 5.40 | Measurement 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." | 5.22 | Changeover 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." | 5.20 | TET2 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)." | 4.31 | Central 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." | 3.91 | PTH 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." | 3.83 | Endogenous 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." | 3.83 | Cortisol/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." | 3.83 | Cholecalciferol 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)." | 3.81 | Serum 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)." | 3.79 | Quantification 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." | 3.78 | Plasma 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." | 3.01 | The Effect of Aldosterone on Cardiorenal and Metabolic Systems. ( Abe, M; Kobayashi, H; Otsuka, H, 2023) |
"Aldosterone has hypertrophic and profibrotic effects on the heart." | 1.91 | Serum 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." | 1.62 | Modulation 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." | 1.62 | Hemodynamic 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)." | 1.62 | Aldosterone 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." | 1.56 | Renin-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." | 1.51 | Aldosterone 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." | 1.48 | Criteria 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." | 1.48 | Confirmatory 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." | 1.48 | Inflammation 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." | 1.48 | Aldosterone 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)." | 1.48 | Microvascular 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." | 1.46 | Increased 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." | 1.46 | Plasma 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." | 1.42 | Prevalence 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." | 1.42 | Circulating 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." | 1.42 | Clinical 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." | 1.42 | Plasma 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." | 1.42 | Decreased 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)." | 1.40 | Primary 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." | 1.40 | Oxidative 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." | 1.40 | Measurement 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) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 17 (17.71) | 18.7374 |
1990's | 0 (0.00) | 18.2507 |
2000's | 0 (0.00) | 29.6817 |
2010's | 55 (57.29) | 24.3611 |
2020's | 24 (25.00) | 2.80 |
Authors | Studies |
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Morris, DJ | 1 |
Brem, AS | 1 |
Odermatt, A | 1 |
Petramala, L | 3 |
Concistrè, A | 3 |
Circosta, F | 1 |
Gigante, A | 1 |
Sarlo, F | 1 |
Schina, M | 1 |
Soldini, M | 1 |
Iannucci, G | 2 |
Cianci, R | 1 |
Letizia, C | 3 |
McNally, RJ | 1 |
Morselli, F | 1 |
Farukh, B | 1 |
Chowienczyk, PJ | 1 |
Faconti, L | 1 |
Chen, PT | 2 |
Chang, D | 1 |
Liu, KL | 2 |
Liao, WC | 1 |
Wang, W | 2 |
Chang, CC | 5 |
Wu, VC | 10 |
Lin, YH | 11 |
Chang, CM | 1 |
Peng, KY | 2 |
Chan, CK | 2 |
Lin, YF | 1 |
Liao, HW | 1 |
Chang, JG | 1 |
Wu, MS | 1 |
Chang, WC | 1 |
Han, L | 1 |
Xu, XJ | 1 |
Zhang, JS | 1 |
Liu, HM | 1 |
Hu, YH | 2 |
Lai, TS | 1 |
Wang, SM | 2 |
Lu, CC | 1 |
Liu, YC | 1 |
Tsai, YC | 3 |
Chueh, JS | 1 |
Al-Hashedi, EM | 1 |
Zhao, X | 1 |
Mohammed, AA | 1 |
Juvenal, H | 1 |
Yu, J | 1 |
Gomez-Sanchez, CE | 1 |
Gomez-Sanchez, EP | 1 |
Otsuka, H | 2 |
Abe, M | 2 |
Kobayashi, H | 4 |
Kishimoto, S | 2 |
Oki, K | 2 |
Maruhashi, T | 2 |
Kajikawa, M | 2 |
Mizobuchi, A | 1 |
Harada, T | 1 |
Yamaji, T | 1 |
Hashimoto, Y | 1 |
Yoshimura, K | 1 |
Nakano, Y | 1 |
Goto, C | 1 |
Yusoff, FM | 2 |
Nakashima, A | 1 |
Higashi, Y | 3 |
Li, J | 2 |
Yang, N | 1 |
Chou, H | 1 |
Shi, L | 2 |
Wei, M | 1 |
Li, Y | 2 |
Burrello, J | 1 |
Buffolo, F | 1 |
Domenig, O | 1 |
Tetti, M | 1 |
Pecori, A | 1 |
Monticone, S | 1 |
Poglitsch, M | 1 |
Mulatero, P | 1 |
Libianto, R | 1 |
Fuller, PJ | 1 |
Young, MJ | 1 |
Yang, J | 1 |
Liu, Y | 2 |
Lin, Y | 1 |
Zhang, MM | 1 |
Li, XH | 1 |
Liu, YY | 1 |
Zhao, J | 1 |
Zhang, SL | 1 |
Gao, JW | 1 |
Guo, Y | 1 |
Feng, QL | 1 |
Tang, JY | 1 |
Yan, L | 1 |
Wang, JF | 1 |
Cheng, H | 1 |
Liu, PM | 1 |
Fuss, CT | 1 |
Brohm, K | 1 |
Kurlbaum, M | 1 |
Hannemann, A | 1 |
Kendl, S | 1 |
Fassnacht, M | 1 |
Deutschbein, T | 2 |
Hahner, S | 1 |
Kroiss, M | 1 |
Chu, HT | 1 |
Li, L | 1 |
Jia, M | 1 |
Diao, LL | 1 |
Li, ZB | 1 |
van der Heijden, CDCC | 1 |
Smeets, EMM | 1 |
Aarntzen, EHJG | 1 |
Wesseling, M | 1 |
de Jager, SCA | 1 |
Riksen, NP | 1 |
Teruyama, K | 1 |
Naruse, M | 2 |
Tsuiki, M | 1 |
Pan, CT | 2 |
Wu, XM | 4 |
Tsai, CH | 1 |
Chang, YY | 5 |
Chen, ZW | 3 |
Lee, BC | 2 |
Liao, CW | 4 |
Chen, YL | 1 |
Lin, LC | 2 |
Chang, YR | 1 |
Hung, CS | 6 |
Gideon, A | 1 |
Sauter, C | 1 |
Ehlert, U | 1 |
von Känel, R | 1 |
Wirtz, PH | 1 |
Chen, KM | 1 |
Lin, KH | 1 |
Wu, TH | 1 |
Hong, JS | 1 |
Moon, SJ | 1 |
Jang, HN | 1 |
Kim, JH | 1 |
Moon, MK | 1 |
Ruilope, LM | 1 |
Tamargo, J | 1 |
Spannella, F | 1 |
Giulietti, F | 1 |
Balietti, P | 1 |
Borioni, E | 1 |
Lombardi, FE | 1 |
Ricci, M | 1 |
Cocci, G | 1 |
Landi, L | 1 |
Sarzani, R | 1 |
Haase, M | 1 |
Dringenberg, T | 1 |
Allelein, S | 1 |
Willenberg, HS | 1 |
Schott, M | 1 |
Huang, KC | 1 |
Lee, JK | 2 |
Chen, CW | 2 |
Wu, C | 1 |
Zhang, H | 2 |
Zhang, J | 2 |
Xie, C | 1 |
Fan, C | 1 |
Wu, P | 1 |
Wei, Q | 1 |
Tan, W | 1 |
Xu, L | 1 |
Wang, L | 1 |
Xue, Y | 1 |
Guan, M | 1 |
Song, Y | 2 |
Yang, S | 2 |
He, W | 2 |
Hu, J | 2 |
Cheng, Q | 2 |
Wang, Y | 1 |
Luo, T | 1 |
Ma, L | 1 |
Zhen, Q | 2 |
Zhang, S | 1 |
Mei, M | 1 |
Wang, Z | 2 |
Qing, H | 1 |
Bruemmer, D | 1 |
Peng, B | 1 |
Li, Q | 2 |
Meng, X | 1 |
Wang, X | 1 |
Yu, Y | 1 |
Chou, CH | 2 |
Wei, LH | 1 |
Shun, CT | 1 |
Wen, WF | 1 |
Wan, CH | 1 |
Wu, KD | 4 |
Baron, S | 1 |
Amar, L | 1 |
Faucon, AL | 1 |
Blanchard, A | 1 |
Baffalie, L | 1 |
Faucard, C | 1 |
Travers, S | 1 |
Pagny, JY | 1 |
Azizi, M | 1 |
Houillier, P | 1 |
Davogustto, G | 1 |
Wang, TJ | 1 |
Gupta, DK | 1 |
Ohno, Y | 1 |
Sone, M | 1 |
Inagaki, N | 1 |
Yamasaki, T | 1 |
Ogawa, O | 1 |
Takeda, Y | 1 |
Kurihara, I | 1 |
Umakoshi, H | 1 |
Ichijo, T | 1 |
Katabami, T | 1 |
Wada, N | 2 |
Ogawa, Y | 1 |
Yoshimoto, T | 1 |
Kawashima, J | 1 |
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Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
LC-MS/MS-specific Cutoffs for Screening and Confirmatory Testing of Primary Aldosteronism: A Multi-center Study[NCT05959863] | 300 participants (Anticipated) | Observational | 2023-08-30 | Recruiting | |||
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 2 | 63 participants (Actual) | Interventional | 2009-01-14 | Completed | ||
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 2 | 628 participants (Actual) | Interventional | 2008-09-11 | Completed | ||
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 2 | 155 participants (Actual) | Interventional | 2008-12-22 | Completed | ||
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 2 | 12 participants (Anticipated) | Interventional | 2008-06-30 | Completed | ||
Increasing Stay-on-therapy in Hypertensive Patients Treated With First-line Diuretics: An Active Pharmacosurveillance and Pharmacogenetic Study.[NCT00408512] | Phase 4 | 2,500 participants (Anticipated) | Interventional | 2006-12-31 | Completed | ||
Hypertension in High School Students: Genetic and Environmental Factors[NCT06049641] | 2,638 participants (Actual) | Observational | 2014-10-31 | Completed | |||
Technology Assisted Management of Uncontrolled Hypertension (TEAM-HTN): a Pilot Study[NCT03281772] | 180 participants (Anticipated) | Observational | 2017-01-24 | Recruiting | |||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
(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
Intervention | hr (Geometric Mean) |
---|---|
Cohort A: LCI699 0.5 mg QD | 4.67 |
Cohort A: LCI699 1.0 mg QD | 3.79 |
Cohort B1: LCI699 1.0 mg BID | 5.52 |
Cohort B1: LCI699 2.0 mg QD | 4.90 |
(NCT00817414)
Timeframe: Day 42: Pre-dose and 0.5, 1, 2, 3, 4, and 8-hours post-dose
Intervention | nanogram*hour per milliliter (ng*hr/mL) (Geometric Mean) |
---|---|
Cohort A: LCI699 0.5 mg QD | 6.60 |
Cohort A: LCI699 1.0 mg QD | 14.1 |
Cohort B1: LCI699 1.0 mg BID | 24.1 |
Cohort B1: LCI699 2.0 mg QD | 46.4 |
(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
Intervention | ng*hr/mL (Geometric Mean) |
---|---|
Cohort A: LCI699 0.5 mg QD | 9.23 |
Cohort A: LCI699 1.0 mg QD | 18.8 |
Cohort B1: LCI699 1.0 mg BID | 30.6 |
Cohort B1: LCI699 2.0 mg QD | 68.9 |
(NCT00817414)
Timeframe: Predose and 3 hours post-dose on Day 7
Intervention | nanogram per milliliter (ng/mL) (Geometric Mean) |
---|---|
Cohort A: LCI699 0.5 mg QD | 1.51 |
Cohort A: LCI699 1.0 mg QD | 2.88 |
Cohort B1: LCI699 1.0 mg BID | 3.92 |
Cohort B1: LCI699 2.0 mg QD | 6.73 |
(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
Intervention | ng/mL (Geometric Mean) |
---|---|
Cohort A: LCI699 0.5 mg QD | 1.42 |
Cohort A: LCI699 1.0 mg QD | 2.94 |
Cohort B1: LCI699 1.0 mg BID | 4.62 |
Cohort B1: LCI699 2.0 mg QD | 8.86 |
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
Intervention | milligrams (mg) (Number) |
---|---|
LCI699 | 1.30 |
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
Intervention | Participants (Count of Participants) |
---|---|
Cohort A: LCI699 0.5 mg QD | 6 |
Cohort A: LCI699 1 mg QD | 9 |
Cohort B1: LCI699 1 mg BID | 10 |
Cohort B1: LCI699 2 mg QD | 10 |
Placebo | 10 |
(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
Intervention | hour (hr) (Median) |
---|---|
Cohort A: LCI699 0.5 mg QD | 2.21 |
Cohort A: LCI699 1.0 mg QD | 1.00 |
Cohort B1: LCI699 1.0 mg BID | 1.00 |
Cohort B1: LCI699 2.0 mg QD | 1.00 |
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
Intervention | nanomoles per liter (nmol/L) (Mean) | ||
---|---|---|---|
Day 7 | Day 28 | Day 42 | |
Cohort A: LCI699 0.5 mg QD | 690.0 | 634.87 | 647.51 |
Cohort A: LCI699 1.0 mg QD | 669.40 | 573.41 | 626.08 |
Cohort B1: LCI699 1.0 mg BID | 625.06 | 554.79 | 539.68 |
Cohort B1: LCI699 2.0 mg QD | 562.04 | 539.09 | 479.91 |
Placebo | 799.06 | 804.86 | 812.91 |
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
Intervention | percentage of participants (Number) | |
---|---|---|
MSDBP Response | MSDBP Control | |
Cohort A: LCI699 0.5 mg QD | 58.3 | 58.3 |
Cohort A: LCI699 1 mg QD | 66.7 | 66.7 |
Cohort B1: LCI699 1 mg BID | 100 | 76.9 |
Cohort B1: LCI699 2 mg QD | 76.9 | 76.9 |
Placebo | 61.5 | 46.2 |
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
Intervention | percentage of participants (Number) | |
---|---|---|
MSSBP Response | MSSBP Control | |
Cohort A: LCI699 0.5 mg QD | 58.3 | 50.0 |
Cohort A: LCI699 1 mg QD | 50.0 | 41.7 |
Cohort B1: LCI699 1 mg BID | 69.2 | 61.5 |
Cohort B1: LCI699 2 mg QD | 76.9 | 76.9 |
Placebo | 61.5 | 53.8 |
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
Intervention | mm 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: Placebo | 1.03 |
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
Intervention | mm 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: Placebo | 1.11 |
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
Intervention | mm 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 |
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
Intervention | mm 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 |
Change from baseline was analyzed using plasma aldosterone values measured at Baseline and Week 8. (NCT00758524)
Timeframe: Baseline, Week 8
Intervention | picomoles 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 BID | 277.1 |
Core Period: Placebo | -28.8 |
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
Intervention | nanomoles per liter (nmol/L) (Mean) |
---|---|
Core Period: LCI699 0.25 mg QD | 729.20 |
Core Period: LCI699 0.5 mg QD | 692.74 |
Core Period: LCI699 1.0 mg QD | 604.46 |
Core Period: LCI699 0.5 mg BID | 609.21 |
Core Period: Eplerenone 50 mg BID | 802.32 |
Core Period: Placebo | 822.65 |
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
Intervention | mm 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 |
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
Intervention | mm 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 |
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
Intervention | mm Hg (Least Squares Mean) |
---|---|
Withdrawal Period: LCI699 0.25 mg QD | 0.5 |
Withdrawal Period: LCI699 0.25 mg QD Placebo | 0.5 |
Withdrawal Period: LCI699 0.5 mg QD | 1.6 |
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 Placebo | 2.5 |
Withdrawal Period: LCI699 0.5 mg BID | 1.3 |
Withdrawal Period: LCI699 0.5 mg BID Placebo | 1.3 |
Withdrawal Period: Eplerenone 50 mg BID | -1.2 |
Withdrawal Period: Eplerenone 50 mg BID Placebo | 0.4 |
Withdrawal Period: Placebo | 1.6 |
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
Intervention | mm Hg (Least Squares Mean) |
---|---|
Withdrawal Period: LCI699 0.25 mg QD | 0.3 |
Withdrawal Period: LCI699 0.25 mg QD Placebo | 3.3 |
Withdrawal Period: LCI699 0.5 mg QD | 0.5 |
Withdrawal Period: LCI699 0.5 mg QD Placebo | 2.5 |
Withdrawal Period: LCI699 1.0 mg QD | 0.4 |
Withdrawal Period: LCI699 1.0 mg QD Placebo | 5.3 |
Withdrawal Period: LCI699 0.5 mg BID | 1.6 |
Withdrawal Period: LCI699 0.5 mg BID Placebo | 4.4 |
Withdrawal Period: Eplerenone 50 mg BID | -1.5 |
Withdrawal Period: Eplerenone 50 mg BID Placebo | 2.7 |
Withdrawal Period: Placebo | 1.8 |
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
Intervention | Participants (Count of Participants) | ||
---|---|---|---|
AEs | SAEs | Deaths | |
Core Period: Eplerenone 50 mg BID | 26 | 0 | 0 |
Core Period: LCI699 0.25 mg QD | 23 | 1 | 0 |
Core Period: LCI699 0.5 mg BID | 27 | 0 | 0 |
Core Period: LCI699 0.5 mg QD | 22 | 0 | 0 |
Core Period: LCI699 1.0 mg QD | 24 | 0 | 0 |
Core Period: Placebo | 23 | 1 | 0 |
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
Intervention | percentage of participants (Number) | |
---|---|---|
MSDBP Response | MSDBP Control | |
Core Period: Eplerenone 50 mg BID | 48.8 | 45.2 |
Core Period: LCI699 0.25 mg QD | 39.1 | 32.6 |
Core Period: LCI699 0.5 mg BID | 34.4 | 29.2 |
Core Period: LCI699 0.5 mg QD | 34.1 | 29.4 |
Core Period: LCI699 1.0 mg QD | 50.0 | 41.9 |
Core Period: Placebo | 27.6 | 18.4 |
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
Intervention | percentage of participants (Number) | |
---|---|---|
MSSBP Response | MSSBP Control | |
Core Period: Eplerenone 50 mg BID | 52.4 | 44.0 |
Core Period: LCI699 0.25 mg QD | 39.1 | 31.5 |
Core Period: LCI699 0.5 mg BID | 34.4 | 25.0 |
Core Period: LCI699 0.5 mg QD | 37.6 | 27.1 |
Core Period: LCI699 1.0 mg QD | 48.8 | 40.7 |
Core Period: Placebo | 17.1 | 15.8 |
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
Intervention | ratio (Least Squares Mean) | |||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Week 8, Hour 1 | Week 8, Hour 2 | Week 8, Hour 3 | Week 8, Hour 4 | Week 8, Hour 5 | Week 8, Hour 6 | Week 8, Hour 7 | Week 8, Hour 8 | Week 8, Hour 9 | Week 8, Hour 10 | Week 8, Hour 11 | Week 8, Hour 12 | Week 8, Hour 13 | Week 8, Hour 14 | Week 8, Hour 15 | Week 8, Hour 16 | Week 8, Hour 17 | Week 8, Hour 18 | Week 8, Hour 19 | Week 8, Hour 20 | Week 8, Hour 21 | Week 8, Hour 22 | Week 8, Hour 23 | Week 8, Hour 24 | |
Core Period: Eplerenone 50 mg BID | 0.17 | -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 QD | 3.91 | 1.44 | 1.16 | 0.51 | 1.11 | -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 BID | 3.87 | 3.44 | 4.01 | 2.64 | 1.45 | 1.20 | 1.21 | 2.09 | 3.27 | 0.49 | 1.54 | -1.06 | -1.45 | -2.96 | -6.10 | -9.54 | -10.38 | -11.85 | -10.78 | -10.49 | -8.22 | -6.35 | -2.67 | 1.36 |
Core Period: LCI699 0.5 mg QD | 2.95 | 1.85 | 1.13 | 2.91 | -0.02 | -2.36 | -0.95 | -1.38 | -0.07 | 2.60 | 1.72 | 2.53 | -1.20 | -3.29 | -5.82 | -8.37 | -10.99 | -11.73 | -10.12 | -8.06 | -7.68 | -4.93 | -1.93 | 1.45 |
Core Period: LCI699 1.0 mg QD | 0.27 | 0.17 | -0.36 | 0.35 | -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 | -1.18 | 0.29 |
Core Period: Placebo | 7.11 | 6.28 | 4.99 | 7.02 | 4.31 | 1.82 | 3.62 | 2.65 | 3.30 | 3.86 | 2.38 | 3.24 | 1.52 | -0.90 | -1.01 | -1.61 | -4.20 | -6.89 | -5.84 | -5.21 | -4.12 | -1.09 | 1.82 | 1.98 |
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
Intervention | ratio (Least Squares Mean) | |||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Week 8, Hour 1 | Week 8, Hour 2 | Week 8, Hour 3 | Week 8, Hour 4 | Week 8, Hour 5 | Week 8, Hour 6 | Week 8, Hour 7 | Week 8, Hour 8 | Week 8, Hour 9 | Week 8, Hour 10 | Week 8, Hour 11 | Week 8, Hour 12 | Week 8, Hour 13 | Week 8, Hour 14 | Week 8, Hour 15 | Week 8, Hour 16 | Week 8, Hour 17 | Week 8, Hour 18 | Week 8, Hour 19 | Week 8, Hour 20 | Week 8, Hour 21 | Week 8, Hour 22 | Week 8, Hour 23 | Week 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 | -0.57 | 0.91 | 1.50 | -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 QD | 0.09 | 0.15 | -1.53 | -1.18 | -3.09 | -3.12 | -2.10 | -4.69 | -1.59 | -0.30 | -0.43 | 0.73 | -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: Placebo | 8.23 | 6.48 | 4.60 | 4.68 | 2.78 | 1.42 | 2.25 | 3.76 | 2.39 | 2.54 | 3.51 | 4.69 | 3.20 | 0.75 | 0.02 | -0.33 | -3.03 | -6.35 | -6.98 | -6.53 | -3.89 | -0.94 | 2.18 | 0.70 |
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
Intervention | mmHg (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 |
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
Intervention | mmHg (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 |
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
Intervention | mmHg (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 |
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
Intervention | mmHg (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 |
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
Intervention | Participants (Count of Participants) |
---|---|
LCI699 0.25 mg BID | 0 |
LCI699 1 mg QD | 1 |
LCI699 0.5 mg Followed by LCI699 1 mg BID | 4 |
Eplerenone 50 mg BID | 0 |
Placebo | 0 |
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
Intervention | percent change in ARC (Geometric Least Squares Mean) |
---|---|
LCI699 0.25 mg BID | 73.1 |
LCI699 1 mg QD | 72.8 |
LCI699 0.5 mg Followed by LCI699 1 mg BID | 156.4 |
Eplerenone 50 mg BID | 430.6 |
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
Intervention | percent change in PRA (Geometric Least Squares Mean) |
---|---|
LCI699 0.25 mg BID | 41.6 |
LCI699 1 mg QD | 74.3 |
LCI699 0.5 mg Followed by LCI699 1 mg BID | 107.7 |
Eplerenone 50 mg BID | 414.1 |
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
Intervention | percent 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 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
Intervention | percent 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 BID | 115.0 |
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
Intervention | mmHg (Mean) | ||
---|---|---|---|
24-hour Mean DBP | Daytime Mean DBP | Nighttime Mean DBP | |
LCI699 0.5 mg BID | -2.5 | -2.6 | -2.8 |
LCI699 1 mg QD | -4.3 | -3.9 | -4.5 |
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
Intervention | mmHg (Mean) | ||
---|---|---|---|
24-hour Mean DBP | Daytime Mean DBP | Nighttime Mean DBP | |
Eplerenone 50 mg BID | -9.6 | -9.5 | -9.6 |
LCI699 0.25 mg BID | 1.0 | 0.6 | 1.9 |
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 | -0.8 | 1.2 |
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
Intervention | mmHg (Mean) | ||
---|---|---|---|
24-hour Mean SBP | Daytime Mean SBP | Nighttime Mean SBP | |
LCI699 0.5 mg BID | -4.7 | -5.3 | -4.5 |
LCI699 1 mg QD | -7.8 | -8.1 | -6.8 |
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
Intervention | mmHg (Mean) | ||
---|---|---|---|
24-hour Mean SBP | Daytime Mean SBP | Nighttime 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 | -1.6 | 0.4 |
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
Intervention | Participants (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 BID | 13 | 1 | 0 | 0 | 1 | 3 |
LCI699 0.25 mg BID | 15 | 0 | 2 | 2 | 0 | 3 |
LCI699 0.5 mg Followed by LCI699 1 mg BID | 8 | 0 | 0 | 0 | 0 | 7 |
LCI699 1 mg QD | 15 | 0 | 0 | 0 | 0 | 2 |
Placebo | 16 | 0 | 1 | 0 | 0 | 2 |
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
Intervention | percentage of participants (Number) | |
---|---|---|
MSDBP Response | MSDBP Control | |
Eplerenone 50 mg BID | 71.9 | 56.3 |
LCI699 0.25 mg BID | 67.7 | 54.8 |
LCI699 0.5 mg Followed by LCI699 1 mg BID | 71.0 | 58.1 |
LCI699 1 mg QD | 73.1 | 65.4 |
Placebo | 57.6 | 54.5 |
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
Intervention | percentage of participants (Number) | |
---|---|---|
MSSBP Response | MSSBP Control | |
Eplerenone 50 mg BID | 65.6 | 53.1 |
LCI699 0.25 mg BID | 54.8 | 51.6 |
LCI699 0.5 mg Followed by LCI699 1 mg BID | 41.9 | 32.3 |
LCI699 1 mg QD | 57.7 | 50.0 |
Placebo | 42.4 | 36.4 |
7 reviews available for aldosterone and Hypertension, Essential
Article | Year |
---|---|
The Effect of Aldosterone on Cardiorenal and Metabolic Systems.
Topics: Aldosterone; Cardiovascular Diseases; Essential Hypertension; Humans; Hyperaldosteronism; Hypertensi | 2023 |
Primary aldosteronism is a public health issue: challenges and opportunities.
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.
Topics: Adrenal Gland Neoplasms; Aldosterone; Catecholamines; Essential Hypertension; Female; Humans; Male; | 2017 |
Aldosterone and Left Ventricular Remodeling.
Topics: Aldosterone; Essential Hypertension; Heart Ventricles; Humans; Hyperaldosteronism; Hypertension; Ven | 2015 |
MECHANISMS IN ESSENTIAL HYPERTENSION.
Topics: Aldosterone; Angiotensins; Catecholamines; Essential Hypertension; Guanethidine; Hypertension; Miner | 1964 |
[METABOLIC DATA ON HYPERTENSION (ESSENTIAL HYPERTENSION)].
Topics: Adrenal Glands; Aldosterone; Angiotensins; Arteriosclerosis; Autonomic Nervous System Diseases; Cate | 1964 |
[NEW DATA ON THE ETIOPATHOGENESIS OF ESSENTIAL ARTERIAL HYPERTENSION].
Topics: Aldosterone; Electrolytes; Essential Hypertension; Humans; Hypertension; Metabolism | 1965 |
4 trials available for aldosterone and Hypertension, Essential
Article | Year |
---|---|
Aldosterone synthase inhibition for the treatment of hypertension and the derived mechanistic requirements for a new therapeutic strategy.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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).
Topics: Aged; Aldosterone; Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Antihypertensive Agents; | 2016 |
85 other studies available for aldosterone and Hypertension, Essential
Article | Year |
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Modulation of 11β-hydroxysteroid dehydrogenase functions by the cloud of endogenous metabolites in a local microenvironment: The glycyrrhetinic acid-like factor (GALF) hypothesis.
Topics: 11-beta-Hydroxysteroid Dehydrogenases; Aldosterone; Animals; Blood Pressure; Corticosterone; Essenti | 2021 |
Evaluation of Intra-Renal Stiffness in Patients with Primary Aldosteronism.
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.
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.
Topics: Adenoma; Adrenalectomy; Aldosterone; Essential Hypertension; Humans; Hyperaldosteronism; Retrospecti | 2022 |
Divergent Characteristics of T-Cell Receptor Repertoire Between Essential Hypertension and Aldosterone-Producing Adenoma.
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.
Topics: Adult; Aldosterone; Angiotensins; Asian People; Blood Pressure; Essential Hypertension; Female; Huma | 2022 |
Circulating Plasma Concentrations of ACE2 in Primary Aldosteronism and Cardiovascular Outcomes.
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.
Topics: Aldosterone; Diastole; Echocardiography; Essential Hypertension; Female; Humans; Hypertension; Hyper | 2023 |
Aldosterone Synthase Inhibitors and the Treatment of Essential Hypertension.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Topics: Aldosterone; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension; Radioimmunoassay; Ren | 2022 |
Hemodynamic and Non-Hemodynamic Components of Cardiac Remodeling in Primary Aldosteronism.
Topics: Adrenalectomy; Adrenocortical Adenoma; Adult; Aldosterone; Blood Pressure; Echocardiography; Essenti | 2021 |
Aldosterone hyperreactivity to acute psychosocial stress induction in men with essential hypertension.
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.
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.
Topics: Aldosterone; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension; Lipids; Retrospective | 2021 |
Aldosterone a Relevant Factor in the Beginning and Evolution of Arterial Hypertension.
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.
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.
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.
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.
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.
Topics: Adrenal Cortex Function Tests; Adult; Aldosterone; Asian People; Captopril; Essential Hypertension; | 2018 |
IL-6 trans-signalling contributes to aldosterone-induced cardiac fibrosis.
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.
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.
Topics: Aldosterone; Antihypertensive Agents; Atrial Natriuretic Factor; Essential Hypertension; Humans; Hyp | 2018 |
Obesity as a Key Factor Underlying Idiopathic Hyperaldosteronism.
Topics: Adult; Aldosterone; Cross-Sectional Studies; Diabetes Mellitus; Dyslipidemias; Essential Hypertensio | 2018 |
Microvascular endothelial function is impaired in patients with idiopathic hyperaldosteronism.
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.
Topics: Adenoma; Adrenal Hyperplasia, Congenital; Adrenalectomy; Aldosterone; Angiotensin II; Antihypertensi | 2019 |
Subclinical atherosclerosis due to increase of plasma aldosterone concentrations in essential hypertensive individuals.
Topics: Adult; Aldosterone; Ankle Brachial Index; Atherosclerosis; Biomarkers; Carotid Intima-Media Thicknes | 2019 |
Aldosterone Induces Vascular Damage.
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.
Topics: Aldosterone; Cohort Studies; Corticosterone; Cross-Sectional Studies; Essential Hypertension; Female | 2013 |
Aldosterone levels and inflammatory stimulation in essential hypertensive patients.
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.
Topics: Adenoma; Adult; Aged; Aldosterone; Cholesterol, HDL; Creatinine; Dehydroepiandrosterone Sulfate; Ess | 2015 |
Bone health and aldosterone excess.
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.
Topics: Adenoma; Adrenal Gland Neoplasms; Adult; Aldosterone; Creatinine; Essential Hypertension; Female; Hu | 2013 |
Quantification of urinary 18-hydroxycortisol using LC-MS/MS.
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].
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.
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].
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.
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.
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.
Topics: Adult; Aldosterone; Echocardiography; Essential Hypertension; Female; Humans; Hyperaldosteronism; Hy | 2014 |
Oxidative stress in patients affected by primary aldosteronism.
Topics: Adenoma; Adrenalectomy; Adult; Aged; Aldosterone; Essential Hypertension; Female; Humans; Hyperaldos | 2014 |
Decreased plasma prorenin levels in primary aldosteronism: potential diagnostic implications.
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.
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.
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].
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.
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.
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.
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.
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.
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].
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].
Topics: Aldosterone; Asian People; China; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension; | 2016 |
Aldosterone-Renin Ratio and Side-Selective Renal Perfusion in Essential Hypertension.
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.
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.
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.
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.
Topics: Adult; Aldosterone; Biomarkers; Blood Pressure; Epithelial Sodium Channels; Essential Hypertension; | 2017 |
Role of adrenocorticotropic hormone in essential hypertension and primary aldosteronism.
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.
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.
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.
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.
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.
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.
Topics: Adrenalectomy; Aldosterone; Child; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension; | 1959 |
Aldosterone excretion in essential hypertension.
Topics: Aldosterone; Biological Transport; Body Fluids; Essential Hypertension; Humans; Hypertension | 1960 |
[Urinary excretion of aldosterone in essential hypertension. Investigations by a chemical method].
Topics: Aldosterone; Body Fluids; Essential Hypertension; Humans; Hypertension | 1960 |
[Conn's syndrome and essential arterial hypertension].
Topics: Aldosterone; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension | 1960 |
Essential hypertension and aldosterone.
Topics: Aldosterone; Essential Hypertension; Humans; Hypertension | 1961 |
[Natruresis and aldosterone excretion in essential hypertension].
Topics: Aldosterone; Biological Transport; Body Fluids; Essential Hypertension; Humans; Hypertension; Sodium | 1959 |
Surgical treatment of hypertension -- primary aldosteronism. A review of 13 cases.
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.
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.
Topics: Adrenocorticotropic Hormone; Aldosterone; Diet; Essential Hypertension; Humans; Hypertension; Nutrit | 1962 |
Humoral factors in essential hypertension.
Topics: Aldosterone; Essential Hypertension; Humans; Hypertension; Renin | 1963 |
[Intervention of aldosterone and electrolytes in the pathogenesis of essential hypertension].
Topics: Aldosterone; Electrolytes; Essential Hypertension; Humans; Hyperaldosteronism; Hypertension; Sodium; | 1962 |
BLOOD VOLUME, TOTAL BODY WATER AND ALDOSTERONE EXCRETION IN ESSENTIAL HYPERTENSION.
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
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)].
Topics: Aldosterone; Blood Circulation Time; Blood Pressure; Blood Pressure Determination; Blood Volume; Chl | 1962 |