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Journal of Renin-Angiotensin-Aldosterone System
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Prevention and Reversal by Enalapril of Target Organ Damage in Angiotensin II Hypertension

Caroline Rugale

Groupe Rein et Hypertension, Université Montpellier I, Montpellier, France

Magali Cordaillat

Groupe Rein et Hypertension, Université Montpellier I, Montpellier, France

Albert Mimran

Groupe Rein et Hypertension, Université Montpellier I, Montpellier, France

Bernard Jover

Groupe Rein et Hypertension, Université Montpellier I, Montpellier, France, jover{at}iurc.montp.inserm.fr

Angiotensin-converting enzyme inhibitors (ACE-Is) prevent target organ damage in several models of hypertension. The aim of this study was to assess the influence of the ACE-I enalapril (10 mg/kg-1 per day, gavage) on the cardiovascular alterations and production of free radicals induced by chronic infusion of angiotensin II (Ang II, 200 ng/kg-1 per minute, SC) in Sprague-Dawley rats. Enalapril was given concomitantly for the 10 days of Ang II infusion (prevention) or from day 10 to 17 of Ang II infusion (intervention). The influence of the NADPH oxidase inhibitor apocynin (600 mg/L-1 in drinking water) was evaluated. mg/L-l in drinking water) was evaluated. Enalapril and apocynin had no effect on hypertension in the prevention and intervention studies. Enalapril prevented the increase in heart weight index (HWI), carotid cross-sectional area (CSA) and albuminuria induced by Ang II. Enalapril reduced HWI and albuminuria whereas CSA I was not affected in the intervention study. Apocynin had effects comparable to enalapril. Both enalapril and apocynin reduced the overproduction of superoxide anion by the left ventricle and rise in advanced oxidation protein products induced by C Ang II. Therefore, the antioxidant but not the antihypertensive effect of enalapril may participate in the prevention and treatment of the Ang II-induced cardiovascular and renal alterations.

Key Words: ACE inhibitors (ACE-Is) • Cardiac hypertrophy • Proteinuria • Oxidative stress • NADPH oxidase

Journal of Renin-Angiotensin-Aldosterone System, Vol. 6, No. 3, 154-160 (2005)
DOI: 10.3317/jraas.2005.023
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