BETA-ADRENOCEPTOR ACTIVATES ENDOTHELIUM-DEPENDENT RELEASE OF NITRIC-OXIDE IN RAT AORTA

AIM: To examine the possible role of agents elevating cAMP to release NO from aortic endothelial cells. METHODS: N-G-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, partially inhibited endot helium-dependent relaxation evoked in phenylephrine-precontracted ring s by isoproterenol and abolished relaxation mediated by forskolin 0.2 mu mol L(-1). RESULTS: In rings without endothelium, isoproterenol and forskolin were less effective relaxants and L-NAME had no effect on t he responses. In methylene blue-treated rings isoproterenol- and forsk olin-induced relaxation were prevented in both endothelium-intact and -denuded rings, but the inhibitory effects of methylene blue were sign ificantly more in rings with endothelium than in those without. On the other hand, relaxation induced by sodium nitroprusside was not inhibi ted by L-NAME, but was inhibited by methylene blue in both the endothe lium-intact and -denuded rings. The concentration-relaxation curves to sodium nitroprusside after methylene blue were identical for rings wi th and without endothelium. CONCLUSION: beta-Adrenoceptors or any agen t which raises cAMP elevate NO release from endothelial cells.