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The angiotensin-II (AT-II) receptor blocker olmesartan reduces renal damage in animal models of hypertension and diabetes.
Proc West Pharmacol Soc. 2005; 48:35-8.PW

Abstract

The development of angiotensin receptor blockers (ARBs) has resulted in effective oral treatment for hypertension. One of the most recent members of this therapeutic class is olmesartan medoxomil (OM). The active metabolite, olmesartan, produces insurmountable AT1 receptor blockade and dose-dependently reduces BP. In both experimental and clinical studies, ARBs have been shown to exert renoprotective effects in addition to antihypertensive activity. In an SHR model of hypertensive renal injury, OM (3.0 and 10.0 mg/kg/day) dose-dependently reduced BP but also reduced urinary protein excretion by 65% and 75%, respectively (P < 0.05). Similar doses of OM, in a DOCA-salt hypertensive rat model, did not affect BP but reduced urinary protein excretion by 26% and 39% when compared to control hypertensive animals (P < 0.05). Hypertension is a major pathophysiological determinant of progressive arterial damage that can accelerate the development of diabetic nephropathy. At doses of 0.6 and 6.0 mg/kg/day, OM significantly reduces hypertension associated with type 2 diabetes. These doses of OM reduced BP and dose-dependently reduced proteinuria 31% and 76%, respectively, in hypertensive ZDF rats (P < 0.01). OM also reduced renocortical and renomedulla injury by 19% and 50% at doses of 0.6 and 6.0 mg/kg/day. The glomerular sclerosis index (GSI) was also reduced by 25% and 37% (P < 0.05). Thus, OM improves both functional and morphologic damage associated with diabetic nephropathy. These studies demonstrate that OM, a potent ARB, dose-dependently reduces BP and also provides a dose-related nephroprotective effect in animal models of diabetes. These studies show that the antihypertensive affect of OM is renoprotective but suggest that these renal benefits may also occur independently from a reduction in BP. A further evaluation of the effects of OM in diabetes is warranted.

Authors+Show Affiliations

Pharmacology, Forest Research Institute, Jersey City, NJ 07311, USA. Mchael.Pugsley@frx.comi

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16416656

Citation

Pugsley, Michael K.. "The angiotensin-II (AT-II) Receptor Blocker Olmesartan Reduces Renal Damage in Animal Models of Hypertension and Diabetes." Proceedings of the Western Pharmacology Society, vol. 48, 2005, pp. 35-8.
Pugsley MK. The angiotensin-II (AT-II) receptor blocker olmesartan reduces renal damage in animal models of hypertension and diabetes. Proc West Pharmacol Soc. 2005;48:35-8.
Pugsley, M. K. (2005). The angiotensin-II (AT-II) receptor blocker olmesartan reduces renal damage in animal models of hypertension and diabetes. Proceedings of the Western Pharmacology Society, 48, 35-8.
Pugsley MK. The angiotensin-II (AT-II) Receptor Blocker Olmesartan Reduces Renal Damage in Animal Models of Hypertension and Diabetes. Proc West Pharmacol Soc. 2005;48:35-8. PubMed PMID: 16416656.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The angiotensin-II (AT-II) receptor blocker olmesartan reduces renal damage in animal models of hypertension and diabetes. A1 - Pugsley,Michael K, PY - 2006/1/19/pubmed PY - 2006/2/1/medline PY - 2006/1/19/entrez SP - 35 EP - 8 JF - Proceedings of the Western Pharmacology Society JO - Proc West Pharmacol Soc VL - 48 N2 - The development of angiotensin receptor blockers (ARBs) has resulted in effective oral treatment for hypertension. One of the most recent members of this therapeutic class is olmesartan medoxomil (OM). The active metabolite, olmesartan, produces insurmountable AT1 receptor blockade and dose-dependently reduces BP. In both experimental and clinical studies, ARBs have been shown to exert renoprotective effects in addition to antihypertensive activity. In an SHR model of hypertensive renal injury, OM (3.0 and 10.0 mg/kg/day) dose-dependently reduced BP but also reduced urinary protein excretion by 65% and 75%, respectively (P < 0.05). Similar doses of OM, in a DOCA-salt hypertensive rat model, did not affect BP but reduced urinary protein excretion by 26% and 39% when compared to control hypertensive animals (P < 0.05). Hypertension is a major pathophysiological determinant of progressive arterial damage that can accelerate the development of diabetic nephropathy. At doses of 0.6 and 6.0 mg/kg/day, OM significantly reduces hypertension associated with type 2 diabetes. These doses of OM reduced BP and dose-dependently reduced proteinuria 31% and 76%, respectively, in hypertensive ZDF rats (P < 0.01). OM also reduced renocortical and renomedulla injury by 19% and 50% at doses of 0.6 and 6.0 mg/kg/day. The glomerular sclerosis index (GSI) was also reduced by 25% and 37% (P < 0.05). Thus, OM improves both functional and morphologic damage associated with diabetic nephropathy. These studies demonstrate that OM, a potent ARB, dose-dependently reduces BP and also provides a dose-related nephroprotective effect in animal models of diabetes. These studies show that the antihypertensive affect of OM is renoprotective but suggest that these renal benefits may also occur independently from a reduction in BP. A further evaluation of the effects of OM in diabetes is warranted. SN - 0083-8969 UR - https://www.unboundmedicine.com/medline/citation/16416656/The_angiotensin_II__AT_II__receptor_blocker_olmesartan_reduces_renal_damage_in_animal_models_of_hypertension_and_diabetes_ L2 - https://medlineplus.gov/diabetickidneyproblems.html DB - PRIME DP - Unbound Medicine ER -