Enalapril attenuated left ventricular remodeling and restored baseline papillary muscle tension in rats with myocardial infarction, but did not improve cardiac sympathetic neuronal function or beta-adrenergic responsiveness.
Does enalapril improve sympathetic neuronal function and beta-adrenergic desensitization in rats with heart failure after myocardial infarction?
In a rat model of post-MI heart failure, enalapril attenuates LV remodeling and improves baseline contractility, but these benefits are not mediated by sympathoinhibition or restoration of beta-adrenergic signaling.
One of the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in the treatment of heart failure may derive from sympathoinhibition and the prevention of beta-adrenergic desensitization. However, the roles of these properties in the overall effects of ACE inhibitor are not clear. We studied the effects of chronic enalapril treatment (20 mg/L in drinking water for 12 weeks) on left ventricular (LV) function, cardiac norepinephrine (NE), sympathetic neuronal function assessed by 131I-metaiodobenzylguanidine (MIBG), beta-receptors, and isometric contraction of papillary muscle in rats with myocardial infarction (MI) induced by coronary artery ligation. Decreased LV function in the MI rats was associated with reduced cardiac NE content and MIBG uptake, and severely blunted responses of non-infarcted papillary muscle to isoproterenol, forskolin, and calcium. Enalapril attenuated LV remodeling in association with a reduction of the ventricular loading condition and restored baseline developed tension of non-infarcted papillary muscle to the level of sham-operated rats. However, enalapril did not improve cardiac NE content, MIBG uptake, or inotropic responsiveness to beta-agonists. These results suggest that the major effect of the ACE inhibitor enalapril in the treatment of heart failure is not due to sympathoinhibition or restoration of beta-adrenergic pathway in this model of heart failure.
Igawa et al. (Tue,) conducted a other in Heart failure after myocardial infarction (n=80). Enalapril vs. Untreated was evaluated on Left ventricular remodeling, sympathetic neuronal function, and beta-adrenergic desensitization. Enalapril attenuated left ventricular remodeling and restored baseline papillary muscle tension in rats with myocardial infarction, but did not improve cardiac sympathetic neuronal function or beta-adrenergic responsiveness.