1999CirculationRequires access

Activation of Cardiac Aldosterone Production in Rat Myocardial Infarction

Jean-SébastienSilvestre, ChristopheHeymes, AbdeslamOubénaïssa, ValérieRobert, BrigitteAupetit-Faisant, AlainCarayon, BernardSwynghedauw, ClaudeDelcayre

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Abstract

Background—This study analyzed the regulation and the role of the cardiac steroidogenic system in myocardial infarction (MI). Methods and Results—Seven days after MI, rats were randomized to untreated infarcted group or spironolactone- (20 and 80 mg · kg−1 · d−1), losartan- (8 mg · kg−1 · d−1), spironolactone plus losartan–, and L-NAME– (5 mg · kg−1 · d−1) treated infarcted groups for 25 days. Sham-operated rats served as controls. In the noninfarcted myocardium of the left ventricle (LV), MI raised aldosterone synthase mRNA (the terminal enzyme of aldosterone synthesis) by 2.0-fold and the aldosterone level by 3.7-fold. Conversely, MI decreased 11β-hydroxylase mRNA (the terminal enzyme of corticosterone synthesis) by 2.4-fold and the corticosterone level by 1.9-fold. MI also induced a 1.9-fold increase in cardiac angiotensin II level. Such cardiac regulations were completely prevented by treatment of the infarcted heart with losartan. The MI-induced collagen deposition in noninfarcted LV myocardium was p...

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Background—This study analyzed the regulation and the role of the cardiac steroidogenic system in myocardial infarction (MI). Methods and Results—Seven days after MI, rats were randomized to untreated infarcted group or spironolactone- (20 and 80 mg · kg−1 · d−1), losartan- (8 mg · kg−1 · d−1), spironolactone plus losartan–, and L-NAME– (5 mg · kg−1 · d−1) treated infarcted groups for 25 days. Sham-operated rats served as controls. In the noninfarcted myocardium of the left ventricle (LV), MI raised aldosterone synthase mRNA (the terminal enzyme of aldosterone synthesis) by 2.0-fold and the aldosterone level by 3.7-fold. Conversely, MI decreased 11β-hydroxylase mRNA (the terminal enzyme of corticosterone synthesis) by 2.4-fold and the corticosterone level by 1.9-fold. MI also induced a 1.9-fold increase in cardiac angiotensin II level. Such cardiac regulations were completely prevented by treatment of the infarcted heart with losartan. The MI-induced collagen deposition in noninfarcted LV myocardium was p...

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Available abstract

Background—This study analyzed the regulation and the role of the cardiac steroidogenic system in myocardial infarction (MI). Methods and Results—Seven days after MI, rats were randomized to untreated infarcted group or spironolactone- (20 and 80 mg · kg−1 · d−1), losartan- (8 mg · kg−1 · d−1), spironolactone plus losartan–, and L-NAME– (5 mg · kg−1 · d−1) treated infarcted groups for 25 days. Sham-operated rats served as controls. In the noninfarcted myocardium of the left ventricle (LV), MI raised aldosterone synthase mRNA (the terminal enzyme of aldosterone synthesis) by 2.0-fold and the aldosterone level by 3.7-fold. Conversely, MI decreased 11β-hydroxylase mRNA (the terminal enzyme of corticosterone synthesis) by 2.4-fold and the corticosterone level by 1.9-fold. MI also induced a 1.9-fold increase in cardiac angiotensin II level. Such cardiac regulations were completely prevented by treatment of the infarcted heart with losartan. The MI-induced collagen deposition in noninfarcted LV myocardium was p...

Key concepts: Aldosterone, Spironolactone, Losartan, Internal medicine, Medicine, Aldosterone synthase, Endocrinology, Corticosterone

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