Effect of Subchronic Administration of Captopril on a1-Adrenoceptor Agonist-Induced Contraction of Isolated Aorta in Rat

Angiotensin II is a major endocrine hormone that affects directly both vascular smooth muscle and endothelial cells. Since vascular reactivity to angiotensin II changes in more physiological and pathophysiological conditions, the present study was performed to investigate the effect of intraperitoneal administration of angiotensin-converting enzyme inhibitor and captopril (30 and 50 mg kg-1, once daily for 8 weeks) on contractile response of rat aorta. After 8 weeks, the treated rats were anesthetized, their thoracic aortas were excised and placed in a Petri dish filled with Krebs solution for recording of contraction and relaxation response. The obtained results showed that captopril did not modify body weight gain and food or water intake but contractile response of aortic rings to phenylephrine in treated rats with 30 and 50 mg kg-1 captopril, in the presence of endothelium, decreases about 11-22% and 29-32% (P<0.05-P<0.01), respectively, when compared to the controls. Denuded aortic rings from 30 and 50 mg kg-1 captopril-treated rats showed 11-21% and 7-11% decrease in contractile response, respectively. There was a marked endothelium-dependent relaxation response to acetylcholine in 50 mg kg-1 captopril-treated rats compared to the controls (P<0.05). Endothelium-independent relaxation response to isosorbide dinitrate showed no significant difference in all groups. According to these results, it is suggested that captopril exerts its relaxant effect directly and/or indirectly through endothelium by production and releasing of endothelium-derived relaxing factors