Carvedilol, A Novel Cardiovascular Agent, Inhibits Development of Vascular and Ventricular Hypertrophy in Spontaneously Hypertensive Rats
| Autor: | Eliot H. Ohlstein, Lynne Vickery, Albert Camden, Anthony J. Arleth, Cheng Po Sung, Lawson McCartney, Frank C. Barone |
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| Rok vydání: | 1994 |
| Předmět: |
Male
medicine.medical_specialty Heart disease Physiology Heart Ventricles Carbazoles Administration Oral Hemodynamics Cardiomegaly Muscle Smooth Vascular Muscle hypertrophy Propanolamines Ventricular hypertrophy Rats Inbred SHR Internal medicine Internal Medicine medicine Animals Carvedilol Antihypertensive Agents Aorta Dose-Response Relationship Drug business.industry DNA General Medicine medicine.disease Mesenteric Arteries Rats medicine.anatomical_structure Endocrinology Ventricle Cardiovascular agent Blood Vessels business Artery medicine.drug |
| Zdroj: | Clinical and Experimental Hypertension. 16:163-177 |
| ISSN: | 1525-6006 1064-1963 |
| DOI: | 10.3109/10641969409067947 |
| Popis: | The effects of carvedilol, a novel cardiovascular agent, were evaluated in developing spontaneously hypertensive rats (SHR) for effects on hemodynamics, and the ability to effect the development of left ventricular, and vascular hypertrophy associated with chronic hypertension. Chronic oral administration of low dose carvedilol (20 mg/kg/day) was initiated when rats were 5 weeks of age, and experiments progressed until 14 weeks of age. Carvedilol-treated SHR had significantly reduced systolic blood pressures and heart rates throughout the duration of the experiment, and had significantly reduced ventricle/body weights by approximately 9.0%. Morphologic analysis of tertiary branches of the mesenteric artery revealed that carvedilol-treated SHR had significant reductions in medial cross-sectional area. Carvedilol produced concentration-dependent inhibition of basal [3H]thymidine incorporation in cultured SHR vascular smooth muscle cells, as well as by stimulation produced by PDGF (1 nM), EDGF (1 nM), thrombin (0.5 U/ml), or endothelin-1 (1 nM), indicating that carvedilol had direct anti-mitogenic activity. The present studies demonstrate that low dose carvedilol produced sustained reductions in blood pressure and heart rate in developing SHR that were accompanied by significant inhibition in the development of vascular and myocardial hypertrophy. The morphological changes induced by carvedilol may be mediated by a combination of hemodynamic effects, as well as by direct anti-mitogenic effects on vascular smooth muscle. |
| Databáze: | OpenAIRE |
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