Hypertensive-diabetic cardiomyopathy in rats
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F S Fein1, B E Zola, A Malhotra
1Department of Medicine, Albert Einstein College of Medicine, Bronx, New York.
Insights
Hypertension and diabetes in rats cause cardiac dysfunction. The combination leads to left ventricular hypertrophy, impaired muscle function, and potential cardiomyopathy, suggesting a link to congestive heart failure.
Area of Science:
- Cardiovascular Physiology
- Diabetology
- Hypertension Research
Background:
- Hypertension and diabetes are major risk factors for cardiovascular disease.
- Understanding their combined effects on cardiac function is crucial for disease management.
Purpose of the Study:
- To investigate the impact of hypertension, diabetes, and their combination on cardiac structure and function in rats.
- To elucidate the underlying mechanisms of cardiac dysfunction in these conditions.
Main Methods:
- Studied left ventricular papillary muscle function, action potentials, myosin ATPase activity, and myocardial pathology in control, hypertensive, diabetic, and hypertensive-diabetic rats.
- Assessed cardiac hypertrophy, contractility, relaxation, and electrophysiological properties.
Main Results:
- Hypertensive-diabetic rats showed significant left ventricular hypertrophy, prolonged contraction/relaxation, blunted length-tension relation, and decreased membrane potential.
- Myosin ATPase and V1 isoenzyme content decreased progressively in hypertensive and diabetic rats.
- Myocardial pathology increased with hypertension, while cellular dysfunction was prominent in diabetes.
Conclusions:
- The combination of hypertension-induced myocardial pathology and diabetes-induced cellular dysfunction may lead to cardiomyopathy and congestive heart failure in hypertensive-diabetic rats.
- These findings highlight the detrimental synergistic effects of hypertension and diabetes on the heart.
Abstract:
Left ventricular papillary muscle function, transmembrane action potentials, myosin adenosinetriphosphatase (ATPase) and isoenzyme distribution, and myocardial pathology were studied in hypertensive (H), diabetic (D), hypertensive-diabetic (HD), and control (C) rats. There was approximately 50% relative left ventricular hypertrophy in H and HD rats. Relative lung and liver weights were greater in HD rats. Peak velocity of shortening tended to decrease progressively in H, D, and HD rats. The duration of contraction and relaxation was markedly prolonged in Ds and HDs. The length-developed tension relation was blunted in HDs. The negative inotropic effect of verapamil was similar in all groups. Resting membrane potential and amplitude were decreased in D and HD rats. Action potential duration was increased in H, D, and especially HD rats. The shortening of action potential duration with increased stimulus frequency was greater in H, D, and especially HD rats than in Cs. Left ventricular myosin ATPase and V1 isoenzyme content decreased progressively in H, D, and HD rats. Right ventricular V1 isoenzyme content was not affected in H rats but was markedly decreased in D and HD rats. Left (and right) ventricular pathology was unchanged in rats with diabetes but was increased in rats with hypertension. These data suggest that the combination of myocardial pathology (due to hypertension) and cellular dysfunction (caused mainly by diabetes) may result in cardiomyopathy and congestive heart failure in the HD rat.