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Effect of angiotensin converting enzyme inhibitor on regression in cardiac hypertrophy
N Makino1, H Matsui, K Masutomo
1Department of Bioclimatology and Medicine, Kyushu University, Beppu, Japan.
Insights
Enalapril treatment reduced cardiac hypertrophy, left ventricular mass, and systolic pressure in rats. The drug altered adrenoceptor levels and reduced collagen, indicating specific beneficial effects on the hypertrophied heart.
Area of Science:
- Cardiology
- Pharmacology
- Molecular Biology
Background:
- Cardiac hypertrophy is a significant risk factor for cardiovascular disease.
- Angiotensin-converting enzyme (ACE) inhibitors are commonly used to manage hypertension and its cardiac consequences.
- Understanding the mechanisms of cardiac hypertrophy regression is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the effects of enalapril on cardiac hypertrophy regression in experimental rat models.
- To examine the impact of enalapril on myocardial adrenoceptor expression and extracellular matrix components during hypertrophy regression.
- To elucidate the specific mechanisms underlying enalapril's beneficial effects on the hypertrophied heart.
Main Methods:
- Cardiac hypertrophy was induced in rats via aortic banding.
- Regression of hypertrophy was achieved by administering enalapril (10 mg/kg/day).
- Left ventricular mass, systolic pressure, alpha 1- and beta-adrenoceptor numbers, type III collagen mRNA expression, and collagen content were assessed.
Main Results:
- Enalapril treatment decreased left ventricular mass and systolic pressure in hypertrophied rats.
- The drug reduced alpha 1-adrenoceptors in aortic-banded rats but not in spontaneously hypertensive rats.
- Enalapril decreased beta-adrenoceptors in spontaneously hypertensive rats and reduced type III collagen mRNA and collagen content in both models.
Conclusions:
- Cardiac hypertrophy regression induced by enalapril is not consistently associated with decreased alpha 1-adrenergic receptors.
- Enalapril's beneficial effects on the hypertrophied heart in aortic banding models appear to be specific.
- These findings highlight the complex interplay between ACE inhibition, adrenoceptor regulation, and extracellular matrix remodeling in cardiac hypertrophy regression.
Abstract:
Cardiac hypertrophy in rats was produced by aortic banding for 6 weeks and regression of hypertrophy in these experimental animals was induced by administration of angiotensin converting enzyme inhibitor, enalapril (10 mg/kg/day) for 6 weeks. The left ventricular muscle mass and systolic pressure were decrease upon treating the hypertrophied rats with enalapril. This drug also decreased the number of alpha 1-adrenoceptors in hypertrophied myocardium without any changes in beta-adrenoceptors. The regression of cardiac hypertrophy in spontaneously hypertensive rats by enalapril for 10 weeks was not associated with any alterations in alpha 1-adrenoceptors in hypertrophied myocardium, but was decreased in beta-adrenoceptors. Effects of enalapril on extracellular matrix in the myocardium was also observed in regression of hypertrophy in which the type III collagen mRNA expression and collagen contents were reduced in comparison with those of hypertrophied myocardium. These results indicate that regression of cardiac hypertrophy is not always associated with a decrease in the number of alpha 1-adrenergic receptors and that the beneficial effects of enalapril in the hypertrophied heart in aortic banding animals may be of some specific nature.