ENDOTHELIAL MODULATION OF CONTRACTIONS CAUSED BY OXYHEMOGLOBIN AND N(G)-NITRO-L-ARGININE IN ISOLATED DOG AND MONKEY CEREBRAL-ARTERIES

Background and Purpose: Oxyhemoglobin is a key substance in provoking cerebral vasospasm and a scavenger of nitric oxide. The present study was designed to determine whether suppression of the action of endothe lium-derived nitric oxide is involved in oxyhemoglobin-induced cerebro arterial contraction. Methods: Dog and monkey cerebral artery strips w ith and without endothelium were immersed for isometric tension record ing in modified Ringer-Locke solution aerated with 95% oxygen and 5% c arbon dioxide. Results: N(G)-nitro-L-arginine, a nitric oxide synthase inhibitor, produced concentration-related contraction that was greate r in the strips with intact endothelium than in those denuded of endot helium. The D-enantiomer caused no or only a slight contraction. In th e presence of N(G)-nitro-L-arginine, oxyhemoglobin elicited additional contraction that is comparable to or even greater than that obtained in the absence of the inhibitor. The oxyhemoglobin-induced contraction was attenuated by endothelium denudation. Conclusions: Inhibition of the basal release of nitric oxide from endothelium results in dog and monkey cerebral arterial contraction. However, the inhibition of nitri c oxide action is not a major mechanism involved in oxyhemoglobin-indu ced contraction; other mechanisms, such as the release of prostanoids, appear to be important.