Role of nitric oxide in regulation of basilar artery tone in vivo

Abstract

Previous studies have suggested that nitric oxide (NO) may be a major endothelium-derived relaxing factor in peripheral blood vessels. This study tested the hypotheses that 1) formation of NO from L-arginine contributes to basal tone of cerebral arteries in vivo and 2) dilator responses of cerebral arteries to acetylcholine are dependent on formation of NO. Diameter of the basilar artery was measured through a cranial window in anesthetized rats. Under control conditions, topical application of 10 microM NG-monomethyl-L-arginine (L-NMMA, an arginine analogue that inhibits enzymatic formation of NO), constricted the basilar artery by 11 +/- 1% (means +/- SE). L-Arginine (100 microM), which had no effect on baseline diameter, abolished vasoconstriction in response to L-NMMA. L-Arginine did not alter vasodilation during acetylcholine (1 microM) (11 +/- 2 vs. 12 +/- 2%) or vasoconstriction during serotonin (1 nM) (-15 +/- 3 vs. -16 +/- 2%). L-NMMA (5-10 microM) abolished the dilator response of the basilar artery to acetylcholine but did not alter responses to nitroglycerin (0.01 microM) (24 +/- 4 vs. 20 +/- 3%). The inhibitory effect of L-NMMA on the vasodilator response to acetylcholine was prevented by L-arginine. These studies suggest that synthesis of NO from L-arginine influences resting tone of the basilar artery in vivo. Dilatation of the basilar artery to acetylcholine in vivo appears to be dependent on formation of NO from L-arginine.