Literature DB >> 22014125

Comparative effects of different modes of renin angiotensin system inhibition on hypercholesterolaemia-induced atherosclerosis.

Hong Lu1, Anju Balakrishnan1, Deborah A Howatt1, Congqing Wu1, Richard Charnigo1, Gene Liau1, Lisa A Cassis1, Alan Daugherty1.   

Abstract

BACKGROUND AND
PURPOSE: Inhibition of the renin angiotensin system (RAS) has been consistently demonstrated to reduce atherosclerosis. However, there has been no direct comparison among the three available pharmacological modes of inhibiting the RAS, which are inhibitors of renin, ACE and angiotensin II type 1 receptor. The purpose of this study was to determine the relative effects of these three modes of pharmacological RAS inhibition in reducing atherosclerosis by determining the dose-response relationships. EXPERIMENTAL APPROACH: Male LDL receptor -/- mice were administered either vehicle or any of three doses of aliskiren, enalapril or losartan through s.c. infusion for 12 weeks. All mice were fed a saturated fat-enriched diet during drug infusions. Systolic and diastolic BPs were measured during the study using a non-invasive tail-cuff system. Plasma cholesterol and renin concentrations, atherosclerotic lesions, and renal angiotensin II concentrations were determined at the termination of the study. KEY
RESULTS: Plasma renin concentrations were increased by all three drugs. None of the drugs changed plasma cholesterol concentrations. All drugs produced a dose-related decrease in BP. All three drugs also profoundly reduced atherosclerosis in a dose-dependent manner. The highest dose of each drug markedly attenuated lesion size, with no significant differences between the different drugs. The highest dose of each drug also similarly reduced renal angiotensin II concentrations. CONCLUSION AND IMPLICATIONS: Drugs that inhibit the RAS, irrespective of their mode of inhibition, profoundly affect atherosclerotic lesion development in a dose-dependent manner.
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.

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Year:  2012        PMID: 22014125      PMCID: PMC3372847          DOI: 10.1111/j.1476-5381.2011.01712.x

Source DB:  PubMed          Journal:  Br J Pharmacol        ISSN: 0007-1188            Impact factor:   8.739


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