ADENOSINE ENHANCES NITRIC-OXIDE PRODUCTION BY VASCULAR ENDOTHELIAL-CELLS

Adenosine per se is a potent vasodilator of vascular smooth muscle. En dothelial cells modulate vascular tone via the release of nitric oxide (NO), which also elicits vasodilation. This study was undertaken to d etermine whether adenosine could directly stimulate endothelial cells to enhance NO production, which could subsequently reduce vascular ton e. NO production was evaluated in porcine carotid artery endothelial c ells (PCAEC) and human saphenous vein endothelial cells (HSVEC) seeded on multiwell plates, grown to confluence, and treated with adenosine for 1 h. The bathing medium was collected, and the NO production was d etermined as reflected by the formation of NO2- and NO3-. NO productio n by PCAEC was significantly increased by adenosine in a dose-dependen t manner, whereas there was only an insignificant tendency for an incr ease by HSVEC. The addition of the NO synthase competitive inhibitor, N-G-monomethyl-L-arginine (NMMA), or the adenosine receptor antagonist , theophylline, prevented the increase in NO production by adenosine. The results suggest that adenosine stimulates, by a receptor-mediated mechanism, the production of NO by arterial, but not by venous, endoth elial cells.