To delineate the obligatory role of the endothelium in the relaxation of isolated rabbit renal artery in response to acetylcholine(Ach), the effects of phenylephrine(PE), clonidine(CND) and Ach on the contraction and relaxation of the vessel with or without endothelium were investigated.
Alpha-adrenoceptor agonists, PE and CND contracted the arterial rings with dose-related fashion but Ach, a specific muscarinic agonist, induced the contraction in only higher doses. The contractile responses to the drugs were potentiated by removal of the endothelium. The contraction induced by high KCI, however, was not changed after removal of the endothelium. Pretreatment of diltiazem depressed significantly the CND-induced contraction but did not influence the PE-induced contraction. Ach elicited dose-dependent relaxations in intact endothelial rings precontracted with the drugs. The Ach-induced relaxation was greater in the CND-precontracted ring than in the PE-precontracted one, and both Ach-induced relaxations were abolished by pretreatment with atropine.
These results indicate that contractile responses of renal arterial smooth muscle to PE, CND and Ach are inhibitorily modulated by endothelium-derived relaxing factor(EDRF) from endothelium, and Ach inuuce release of EDRF. From endothelium, and Ach induces release of EDRF acting on muscarinic receptor in the endothelium, and the release of EDRF induced by Ach is closely related to calcium metabolism.
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