Endothelial modulation of contractions caused by oxyhemoglobin and NG-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 endothelium-derived nitric oxide is involved in oxyhemoglobin-induced cerebroarterial contraction.
Methods: Dog and monkey cerebral artery strips with and without endothelium were immersed for isometric tension recording in modified Ringer-Locke solution aerated with 95% oxygen and 5% carbon dioxide.
Results: NG-nitro-L-arginine, a nitric oxide synthase inhibitor, produced concentration-related contraction that was greater in the strips with intact endothelium than in those denuded of endothelium. The D-enantiomer caused no or only a slight contraction. In the presence of NG-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 nitric oxide action is not a major mechanism involved in oxyhemoglobin-induced contraction; other mechanisms, such as the release of prostanoids, appear to be important.