Role of angiotensin in pressure overload-induced hypertrophy in rats: effects of angiotensin-converting enzyme inhibitors, an AT1 receptor antagonist, and surgical reversal
| Autor: | Rajendra Mohabir, Arthur M. Strosberg, Susan D. Young |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Ramipril
Male medicine.medical_specialty Angiotensin receptor Heart Ventricles Tetrazoles Angiotensin-Converting Enzyme Inhibitors Blood Pressure Cardiomegaly Losartan Muscle hypertrophy Rats Sprague-Dawley Renin-Angiotensin System Angiotensin Receptor Antagonists Enalapril Internal medicine Medicine Animals Ventricular Function Aorta Abdominal Pharmacology Pressure overload Angiotensin II receptor type 1 biology business.industry Biphenyl Compounds Body Weight Imidazoles Angiotensin-converting enzyme Organ Size Rats Endocrinology cardiovascular system biology.protein Angiotensin I Cardiology and Cardiovascular Medicine business medicine.drug |
| Zdroj: | Journal of cardiovascular pharmacology. 23(2) |
| ISSN: | 0160-2446 |
| Popis: | The renin-angiotensin system (RAS) has been proposed to play a major role in causing the heart to hypertrophy during pressure overload. We examined whether blockade of this system by the angiotensin-converting enzyme (ACE) inhibitors enalapril (0.5 to 20 mg/kg p.o.) or ramipril (1.0 mg/kg p.o.) or the angiotensin receptor (AT1) antagonist losartan (3.0 mg/kg p.o.) could prevent pressure overload-induced hypertrophy. Pressure overload was produced by abdominal aortic constriction in rats. Cardiac hypertrophy was assessed by an increase in the ratio of left ventricular (LV) weight to body weight and total protein content of the left ventricle. Treatment with enalapril or ramipril, initiated 3 weeks after aortic banding and continued for 3 more weeks, failed to prevent the progression or cause regression of cardiac hypertrophy. Treatment for 6 weeks with ramipril initiated immediately after aortic banding also failed to prevent cardiac hypertrophy. Losartan treatment initiated 3 weeks after aortic banding and continued for 3 more weeks resulted in a slight but significant reduction in the extent of cardiac hypertrophy (45.6% hypertrophy in controls and 35.6% hypertrophy in losartan-treated animals, p < 0.05, n = 11 and 10, respectively). Surgical removal of bands 3 weeks after placement reduced cardiac hypertrophy to a greater extent than that observed in losartan-treated animals. These results suggest that angiotensin may not play a major role in causing pressure overload-induced hypertrophy or in maintaining such hypertrophy. |
| Databáze: | OpenAIRE |
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