losartan has been researched along with Hyperglycemia in 26 studies
Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
losartan : A biphenylyltetrazole where a 1,1'-biphenyl group is attached at the 5-position and has an additional trisubstituted imidazol-1-ylmethyl group at the 4'-position
Hyperglycemia: Abnormally high BLOOD GLUCOSE level.
| Excerpt | Relevance | Reference |
|---|---|---|
| " Therefore, we carried out a randomized, double-blind study to compare the effects of losartan (50 mg QD) and metoprolol (95 mg QD) on insulin sensitivity, insulin secretion, glucose tolerance, and lipids and lipoproteins in 20 hyperinsulinemic subjects with essential hypertension." | 9.08 | Effects of losartan on insulin sensitivity in hypertensive subjects. ( Karjalainen, L; Laakso, M; Lempiäinen-Kuosa, P, 1996) |
| " Captopril and losartan also inhibited hyperglycemia-induced leukostasis at 6 weeks and 1 week in the retinal vasculature, respectively." | 7.74 | Captopril inhibits capillary degeneration in the early stages of diabetic retinopathy. ( Gao, L; Kern, TS; Xi, X; Zhang, JZ, 2007) |
| " In multivariable Cox analyses, adjusting for randomized treatment, age, sex, race, prior anti-hypertensive therapy, baseline uric acid, serum creatinine and glucose entered as standard covariates, and in-treatment non-HDL cholesterol, Cornell product left ventricular hypertrophy, diastolic and systolic pressure, BMI, hydrochlorothiazide and statin use as time-varying covariates, the lowest quartile of in-treatment HDL remained associated with a nearly 9-fold increased risk of new diabetes (hazard ratio 8." | 5.17 | In-treatment HDL cholesterol levels and development of new diabetes mellitus in hypertensive patients: the LIFE Study. ( Dahlöf, B; Devereux, RB; Hille, DA; Kjeldsen, SE; Lindholm, LH; Okin, PM; Wiik, BP, 2013) |
| " Therefore, we carried out a randomized, double-blind study to compare the effects of losartan (50 mg QD) and metoprolol (95 mg QD) on insulin sensitivity, insulin secretion, glucose tolerance, and lipids and lipoproteins in 20 hyperinsulinemic subjects with essential hypertension." | 5.08 | Effects of losartan on insulin sensitivity in hypertensive subjects. ( Karjalainen, L; Laakso, M; Lempiäinen-Kuosa, P, 1996) |
| " In other rats, glucose, insulin, uric acid, and insulin sensitivity index, were determined before and after fructose or lipoic acid plus fructose." | 3.79 | A single oral dose of fructose induces some features of metabolic syndrome in rats: role of oxidative stress. ( Hong, E; Moreno, JA, 2013) |
| " Captopril and losartan also inhibited hyperglycemia-induced leukostasis at 6 weeks and 1 week in the retinal vasculature, respectively." | 3.74 | Captopril inhibits capillary degeneration in the early stages of diabetic retinopathy. ( Gao, L; Kern, TS; Xi, X; Zhang, JZ, 2007) |
| "To determine whether enzymatic p53 glycosylation leads to angiotensin II formation followed by p53 phosphorylation, prolonged activation of the renin-angiotensin system, and apoptosis, ventricular myocytes were exposed to levels of glucose mimicking diabetic hyperglycemia." | 3.71 | Hyperglycemia activates p53 and p53-regulated genes leading to myocyte cell death. ( Anversa, P; Cesselli, D; Fiordaliso, F; Kajstura, J; Leri, A; Limana, F; Nadal-Ginard, B; Safai, B, 2001) |
| "Losartan treatment preserves FRAP levels, reduces DNA oxidative injury and thus the carcinogenesis risk." | 1.42 | Losartan reduces oxidative damage to renal DNA and conserves plasma antioxidant capacity in diabetic rats. ( Bigagli, E; Di Serio, C; Lodovici, M; Raimondi, L; Tarantini, F, 2015) |
| "Obesity is often associated with chronic inflammatory state which contributes to the development of insulin resistance (IR) and type 2 diabetes mellitus (T2DM)." | 1.39 | Comparative study between atorvastatin and losartan on high fat diet-induced type 2 diabetes mellitus in rats. ( El-Moselhy, MA; Heeba, GH; Mourad, AA; Taye, A, 2013) |
| " There was no dose-response effect of losartan." | 1.35 | Regression of glomerular injury by losartan in experimental diabetic nephropathy. ( Fujihara, CK; Machado, FG; Malheiros, DM; Silva, LF; Teles, F; Ventura, BH; Zatz, R, 2009) |
| "Losartan treatment significantly prevented all these changes except STZ-induced hypoinsulinemia." | 1.32 | Effect of chronic treatment with losartan on streptozotocin-induced renal dysfunction. ( Goyal, RK; Murali, B; Umrani, DN, 2003) |
| "Losartan (10 mg/kg) was given daily by gavage to Losartan (L) and Losartan + Chronic Stress (L+CS) groups." | 1.32 | Losartan may prevent the elevation of plasma glucose, corticosterone and catecholamine levels induced by chronic stress. ( Erbas, B; Gürol, AO; Ozek, M; Ozkök, E; Uresin, Y, 2004) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 4 (15.38) | 18.2507 |
| 2000's | 7 (26.92) | 29.6817 |
| 2010's | 14 (53.85) | 24.3611 |
| 2020's | 1 (3.85) | 2.80 |
| Authors | Studies |
|---|---|
| Walke, PB | 1 |
| Bansode, SB | 1 |
| More, NP | 1 |
| Chaurasiya, AH | 1 |
| Joshi, RS | 1 |
| Kulkarni, MJ | 1 |
| de Queiroz, DB | 1 |
| Ramos-Alves, FE | 1 |
| Santos-Rocha, J | 1 |
| Duarte, GP | 1 |
| Xavier, FE | 1 |
| Szkudlarek, A | 1 |
| Pentak, D | 1 |
| Ploch, A | 1 |
| Pożycka, J | 1 |
| Maciążek-Jurczyk, M | 1 |
| Okin, PM | 1 |
| Hille, DA | 1 |
| Wiik, BP | 1 |
| Kjeldsen, SE | 1 |
| Lindholm, LH | 1 |
| Dahlöf, B | 1 |
| Devereux, RB | 1 |
| Manni, ME | 1 |
| Zazzeri, M | 1 |
| Musilli, C | 1 |
| Bigagli, E | 2 |
| Lodovici, M | 2 |
| Raimondi, L | 2 |
| Xue, H | 2 |
| Yuan, P | 2 |
| Ni, J | 2 |
| Li, C | 1 |
| Shao, D | 1 |
| Liu, J | 1 |
| Shen, Y | 1 |
| Wang, Z | 1 |
| Zhou, L | 2 |
| Zhang, W | 1 |
| Huang, Y | 2 |
| Yu, C | 2 |
| Wang, R | 1 |
| Lu, L | 1 |
| Tarantini, F | 1 |
| Di Serio, C | 1 |
| Meyer zum Gottesberge, AM | 1 |
| Massing, T | 1 |
| Sasse, A | 1 |
| Palma, S | 1 |
| Hansen, S | 1 |
| Lee, S | 1 |
| Harris, NR | 1 |
| Teles, F | 1 |
| Machado, FG | 1 |
| Ventura, BH | 1 |
| Malheiros, DM | 1 |
| Fujihara, CK | 1 |
| Silva, LF | 1 |
| Zatz, R | 1 |
| Kim, YH | 1 |
| Ryu, JM | 1 |
| Lee, YJ | 1 |
| Han, HJ | 1 |
| Lu, LM | 1 |
| Day, RT | 1 |
| Cavaglieri, Rde C | 1 |
| Tabatabaimir, H | 1 |
| Mantravadi, V | 1 |
| Lee, MJ | 1 |
| Barnes, JL | 1 |
| Kasinath, BS | 1 |
| Feliers, D | 1 |
| Wong, YC | 1 |
| Sim, MK | 1 |
| Lee, KO | 1 |
| Moreno, JA | 1 |
| Hong, E | 1 |
| Yousif, MH | 1 |
| Dhaunsi, GS | 1 |
| Makki, BM | 1 |
| Qabazard, BA | 1 |
| Akhtar, S | 1 |
| Benter, IF | 1 |
| Mourad, AA | 1 |
| Heeba, GH | 1 |
| Taye, A | 1 |
| El-Moselhy, MA | 1 |
| Murali, B | 1 |
| Umrani, DN | 1 |
| Goyal, RK | 1 |
| Uresin, Y | 1 |
| Erbas, B | 1 |
| Ozek, M | 1 |
| Ozkök, E | 1 |
| Gürol, AO | 1 |
| Chipitsyna, G | 1 |
| Gong, Q | 1 |
| Gray, CF | 1 |
| Haroon, Y | 1 |
| Kamer, E | 1 |
| Arafat, HA | 1 |
| Zhang, JZ | 1 |
| Xi, X | 1 |
| Gao, L | 1 |
| Kern, TS | 1 |
| Sechi, LA | 1 |
| Griffin, CA | 1 |
| Schambelan, M | 1 |
| Laakso, M | 1 |
| Karjalainen, L | 1 |
| Lempiäinen-Kuosa, P | 1 |
| Machado, LJ | 1 |
| Marubayashi, U | 1 |
| Reis, AM | 1 |
| Coimbra, CC | 1 |
| Miller, JA | 1 |
| Fiordaliso, F | 1 |
| Leri, A | 1 |
| Cesselli, D | 1 |
| Limana, F | 1 |
| Safai, B | 1 |
| Nadal-Ginard, B | 1 |
| Anversa, P | 1 |
| Kajstura, J | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Phase 2/3 Study of Effect of AT1RB Versus ACE Inhibitor in Addition to XO Inhibitor on Progression of LV Remodeling and Dysfunction in Diabetic Patients With Acute MI.[NCT01052272] | Phase 2/Phase 3 | 72 participants (Actual) | Interventional | 2005-07-31 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
LVEF is a calculation of heart pump function determined from the volume after complete filling minus the volume after complete contraction divided by the volume after complete filling. A value of 55% or greater is normal. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)
| Intervention | percent (Mean) | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Month 0 (n=17,17,18,18) | Month 6(n=14,11,11,12) | Month 9(n=1,2,0,0) | Month 12(n=12,11,11,11) | Month 15(n=3,2,1,1) | Month 18(n=10,12,8,8) | Month 21(n=3,0,0,1) | Month 24 (n=11,9,8,10) | Month 27 (n=1,1,0,1) | |
| Candesartan Cilexetil | 56.36 | 56.82 | 42.62 | 52.37 | 39.88 | 56.33 | NA | 51.70 | 54.17 |
| Candesartan Cilexetil and Allopurinol | 52.68 | 57.28 | NA | 56.11 | 54.46 | 57.82 | 56.17 | 55.79 | 54.40 |
| Ramipril | 52.19 | 54.20 | 64.98 | 52.76 | 52.13 | 55.02 | 51.27 | 57.18 | 50.73 |
| Ramipril and Allopurinol | 53.37 | 52.80 | NA | 51.74 | 34.89 | 54.05 | NA | 55.59 | NA |
LVEDV/BSA: As an indicator of heart size, the blood volume of the heart is related to the body size. The relation of heart blood volume to body size is more accurate in determining pathology because larger people require a larger heart blood volume. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Diastolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)
| Intervention | ml/m^2 (Mean) | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Month 0 (n=17,17,18,18) | Month 6(n=14,11,11,12) | Month 9(n=1,2,0,0) | Month12(n=12,11,11,11) | Month 15(n=3,2,1,1) | Month 18(n=10,12,8,8) | Month 21(n=3,0,0,1) | Month 24 (n=11,9,8,10) | Month 27 (n=1,1,0,1) | |
| Candesartan Cilexetil | 78.06 | 78.60 | 93.57 | 85.44 | 90.20 | 82.74 | NA | 84.28 | 76.65 |
| Candesartan Cilexetil and Allopurinol | 79.03 | 78.01 | NA | 79.75 | 63.1 | 84.95 | 75.27 | 79.72 | 75.05 |
| Ramipril | 73.03 | 74.10 | 73.23 | 75.34 | 81.19 | 75.28 | 71.99 | 70.46 | 48.68 |
| Ramipril and Allopurinol | 78.52 | 86.13 | NA | 83.95 | 108.25 | 67.96 | NA | 71.63 | NA |
LVESV/BSA: The end systolic volume is the blood volume of the heart at the end of contraction and is an index of the pump function of the heart. This relation to body size is more accurate in determining pathology because larger people require a larger heart blood volume. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)
| Intervention | ml/m^2 (Mean) | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Month 0 (n=17,17,18,18) | Month 6(n=14,11,11,12) | Month 9(n=1,2,0,0) | Month 12(n=12,11,11,11) | Month 15(n=3,2,1,1) | Month 18(n=10,12,8,8) | Month 21(n=3,0,0,1) | Month 24 (n=11,9,8,10) | Month 27 (n=1,1,0,1) | |
| Candesartan Cilexetil | 35.26 | 35.26 | 53.87 | 42.27 | 54.04 | 37.76 | NA | 41.72 | 35.13 |
| Candesartan Cilexetil and Allopurinol | 39.49 | 34.15 | NA | 36.07 | 28.74 | 37.18 | 32.99 | 35.99 | 34.22 |
| Ramipril | 36.20 | 34.77 | 25.64 | 36.82 | 39.42 | 35.30 | 35.23 | 31.17 | 23.98 |
| Ramipril and Allopurinol | 37.91 | 42.88 | NA | 42.34 | 70.48 | 30.39 | NA | 31.56 | NA |
LVED Mass/LVEDV: As an indicator of heart muscle mass and heart blood volume, the mass indexed to end diastolic volume determines whether there is an adequate amount of heart muscle to pump the heart blood volume obtained from a three-dimensional analysis. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Geometry. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)
| Intervention | g/ml (Mean) | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Month 0 (n=17,17,18,18) | Month 6(n=14,11,11,12) | Month 9(n=1,2,0,0) | Month 12(n=12,11,11,11) | Month 15(n=3,2,1,1) | Month 18(n=10,12,8,8) | Month 21(n=3,0,0,1) | Month 24 (n=11,9,8,10) | Month 27 (n=1,1,0,1) | |
| Candesartan Cilexetil | 0.95 | 0.83 | 0.67 | 0.78 | 0.70 | 0.79 | NA | 0.80 | 0.64 |
| Candesartan Cilexetil and Allopurinol | 0.87 | 0.82 | NA | 0.86 | 0.68 | 0.80 | 0.69 | 0.82 | 0.69 |
| Ramipril | 0.92 | 0.87 | 0.75 | 0.84 | 0.81 | 0.79 | 0.95 | 0.84 | 0.93 |
| Ramipril and Allopurinol | 0.86 | 0.71 | NA | 0.72 | 0.57 | 0.83 | NA | 0.80 | NA |
LVED Radius/Wall thickness As an indicator of heart muscle mass and heart volume chamber diameter, the end-diastolic radius indexed to end diastolic wall thickness determines whether there is an adequate amount of heart muscle to pump the heart blood volume obtained from a two-dimensional analysis. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Geometry. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)
| Intervention | unitless (Mean) | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Month 0 (n=17,17,18,18) | Month 6(n=14,11,11,12) | Month 9(n=1,2,0,0) | Month 12(n=12,11,11,11) | Month 15(n=3,2,1,1) | Month 18(n=10,12,8,8) | Month 21(n=3,0,0,1) | Month 24 (n=11,9,8,10) | Month 27 (n=1,1,0,1) | |
| Candesartan Cilexetil | 3.14 | 3.39 | 4.14 | 3.68 | 4.10 | 3.71 | NA | 3.58 | 4.04 |
| Candesartan Cilexetil and Allopurinol | 3.45 | 3.63 | NA | 3.42 | 3.90 | 3.56 | 4.24 | 3.56 | 4.29 |
| Ramipril | 3.23 | 3.32 | 3.42 | 3.43 | 3.44 | 3.60 | 2.92 | 3.46 | 3.12 |
| Ramipril and Allopurinol | 3.57 | 4.04 | NA | 4.01 | 4.57 | 3.60 | NA | 3.61 | NA |
By identifying three points in three different planes in the heart muscle, the maximum shortening is the average of the difference between the distance between these three points at the end of filling of the heart and the end of contraction divided by the length at the end of filling times 100. The maximum shortening is a three dimensional analysis. The higher values indicate a healthy heart. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)
| Intervention | percent of length at end of filling (Mean) | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Month 0 (n=17,17,17,18) | Month 6(n=14,11,10,12) | Month 9(n=1,2,0,0) | Month 12(n=11,11,10,10) | Month 15(n=3,2,1,1) | Month 18(n=10,12,7,8) | Month 21(n=3,0,0,1) | Month 24 (n=11,9,8,10) | Month 27 (n=1,1,0,1) | |
| Candesartan Cilexetil | 16.68 | 17.50 | 19.08 | 17.13 | 16.28 | 17.55 | NA | 16.62 | 20.38 |
| Candesartan Cilexetil and Allopurinol | 16.00 | 18.50 | NA | 18.51 | 16.36 | 17.52 | 17.89 | 17.85 | 16.59 |
| Ramipril | 15.81 | 16.88 | 18.43 | 14.57 | 17.06 | 17.26 | 16.68 | 15.67 | 13.70 |
| Ramipril and Allopurinol | 15.84 | 18.72 | NA | 17.96 | 14.22 | 17.46 | NA | 17.52 | NA |
The Peak Early Filling Rate Normalized to EDV is calculated from the slope of the volume during the early filling of the heart with respect to time. The higher values indicate a very healthy heart muscle and lower values are indicative of a very stiff muscle. This is a measure of LV Diastolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)
| Intervention | 1/sec (Mean) | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Month 0 (n=17,17,18,18) | Month 6(n=14,11,11,12) | Month 9(n=1,2,0,0) | Month 12(n=12,11,11,11) | Month 15(n=3,2,1,1) | Month 18(n=10,12,8,8) | Month 21(n=3,0,0,1) | Month 24 (n=11,9,8,10) | Month 27 (n=1,1,0,1) | |
| Candesartan Cilexetil | 2.01 | 2.02 | 1.13 | 1.90 | 1.48 | 1.93 | NA | 1.65 | 1.10 |
| Candesartan Cilexetil and Allopurinol | 2.0 | 1.98 | NA | 1.77 | 2.28 | 2.05 | 2.50 | 1.82 | 2.15 |
| Ramipril | 1.93 | 1.74 | 2.50 | 1.80 | 2.02 | 1.91 | 1.69 | 2.05 | 1.34 |
| Ramipril and Allopurinol | 2.11 | 2.03 | NA | 1.93 | 1.56 | 1.89 | NA | 1.88 | NA |
3 trials available for losartan and Hyperglycemia
| Article | Year |
|---|---|
In-treatment HDL cholesterol levels and development of new diabetes mellitus in hypertensive patients: the LIFE Study.
Topics: Aged; Antihypertensive Agents; Atenolol; Cholesterol, HDL; Comorbidity; Diabetes Mellitus, Type 2; D | 2013 |
Effects of losartan on insulin sensitivity in hypertensive subjects.
Topics: Antihypertensive Agents; Biphenyl Compounds; Blood Pressure; Double-Blind Method; Fatty Acids, Nones | 1996 |
Impact of hyperglycemia on the renin angiotensin system in early human type 1 diabetes mellitus.
Topics: Adult; Angiotensin II; Angiotensin Receptor Antagonists; Blood Pressure; Cross-Over Studies; Diabete | 1999 |
23 other studies available for losartan and Hyperglycemia
| Article | Year |
|---|---|
Molecular investigation of glycated insulin-induced insulin resistance via insulin signaling and AGE-RAGE axis.
Topics: Animals; CHO Cells; Cricetinae; Cricetulus; Glucose; Glucose Transporter Type 4; Glycation End Produ | 2021 |
Losartan reverses COX-2-dependent vascular dysfunction in offspring of hyperglycaemic rats.
Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Cyclooxygenase 2; Endothelium, Vas | 2017 |
In Vitro Investigation of the Interaction of Tolbutamide and Losartan with Human Serum Albumin in Hyperglycemia States.
Topics: Antihypertensive Agents; Glucose; Glycation End Products, Advanced; Humans; Hyperglycemia; Hypoglyce | 2017 |
Exposure of cardiomyocytes to angiotensin II induces over-activation of monoamine oxidase type A: implications in heart failure.
Topics: Aldehyde Dehydrogenase; Angiotensin II; Animals; Biphenyl Compounds; Catalase; Enzyme Activation; He | 2013 |
H(2)S inhibits hyperglycemia-induced intrarenal renin-angiotensin system activation via attenuation of reactive oxygen species generation.
Topics: Acetophenones; Angiotensin II Type 1 Receptor Blockers; Angiotensinogen; Animals; Blood Glucose; Cel | 2013 |
Losartan reduces oxidative damage to renal DNA and conserves plasma antioxidant capacity in diabetic rats.
Topics: 8-Hydroxy-2'-Deoxyguanosine; Adiponectin; Angiotensin II Type 1 Receptor Blockers; Animals; Antioxid | 2015 |
Zucker diabetic fatty rats, a model for type 2 diabetes, develop an inner ear dysfunction that can be attenuated by losartan treatment.
Topics: Animals; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Hearing Loss; Hyperglycemia; La | 2015 |
Losartan and ozagrel reverse retinal arteriolar constriction in non-obese diabetic mice.
Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Arterioles; Blood Flow Velocity; C | 2008 |
Regression of glomerular injury by losartan in experimental diabetic nephropathy.
Topics: Animals; Antihypertensive Agents; Cell Proliferation; Diabetic Nephropathies; Disease Models, Animal | 2009 |
Fibronectin synthesis by high glucose level mediated proliferation of mouse embryonic stem cells: Involvement of ANG II and TGF-beta1.
Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Angiotensinogen; Animals; Calcium Signaling | 2010 |
Angiotensin AT1 receptor activation mediates high glucose-induced epithelial-mesenchymal transition in renal proximal tubular cells.
Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Angiotensinogen; Animals; Cadherins; Cell L | 2010 |
Acute hyperglycemia rapidly stimulates VEGF mRNA translation in the kidney. Role of angiotensin type 2 receptor (AT2).
Topics: Angiotensin II; Animals; Female; Gene Expression Regulation; Heterogeneous-Nuclear Ribonucleoprotein | 2010 |
Des-aspartate-angiotensin-I and angiotensin IV improve glucose tolerance and insulin signalling in diet-induced hyperglycaemic mice.
Topics: Angiotensin I; Angiotensin II; Animals; Blood Glucose; Cystinyl Aminopeptidase; Dietary Fats; Dietar | 2011 |
A single oral dose of fructose induces some features of metabolic syndrome in rats: role of oxidative stress.
Topics: Administration, Oral; Animals; Blood Glucose; Blood Pressure; Dose-Response Relationship, Drug; Fruc | 2013 |
Characterization of Angiotensin-(1-7) effects on the cardiovascular system in an experimental model of type-1 diabetes.
Topics: Angiotensin I; Angiotensin II; Angiotensin-Converting Enzyme 2; Animals; Captopril; Cardiovascular S | 2012 |
Comparative study between atorvastatin and losartan on high fat diet-induced type 2 diabetes mellitus in rats.
Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Atorvastatin; Cholesterol, LDL; Diabetes Mellitus, | 2013 |
Effect of chronic treatment with losartan on streptozotocin-induced renal dysfunction.
Topics: Animals; Antihypertensive Agents; Blood Pressure; Creatinine; Diabetes Mellitus, Experimental; Diabe | 2003 |
Losartan may prevent the elevation of plasma glucose, corticosterone and catecholamine levels induced by chronic stress.
Topics: Animals; Antihypertensive Agents; Blood Glucose; Chronic Disease; Corticosterone; Epinephrine; Hyper | 2004 |
Induction of monocyte chemoattractant protein-1 expression by angiotensin II in the pancreatic islets and beta-cells.
Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Cell Line, Tumor; Chemokine CCL2; | 2007 |
Captopril inhibits capillary degeneration in the early stages of diabetic retinopathy.
Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; A | 2007 |
The cardiac renin-angiotensin system in STZ-induced diabetes.
Topics: Analysis of Variance; Angiotensin II; Angiotensin Receptor Antagonists; Animals; Biphenyl Compounds; | 1994 |
The hyperglycemia induced by angiotensin II in rats is mediated by AT1 receptors.
Topics: Angiotensin I; Angiotensin II; Angiotensins; Animals; Antihypertensive Agents; Hyperglycemia; Losart | 1998 |
Hyperglycemia activates p53 and p53-regulated genes leading to myocyte cell death.
Topics: Angiotensin II; Animals; Apoptosis; Cells, Cultured; DNA; Gene Expression Regulation; Glycosylation; | 2001 |