Analysis of the potentiating action of N(G)-nitro-L-arginine on the contraction of the dog temporal artery elicited by transmural stimulation of noradrenergic nerves.

Dog temporal artery strips without endothelium responded to transmural electrical stimulation with a contraction which was potentiated by NG-nitro-L-arginine (L-NNA). The noradrenaline-induced contraction and the release of 3H-noradrenaline were not affected. The stimulation-induced contraction was reversed to a relaxation by phentolamine. The relaxation was not influenced by timolol and atropine but inhibited by L-NNA; L-arginine abolished the inhibition. Transmural stimulation released NOx from the arteries, the release being abolished by L-NNA. Potentiation by L-NNA of the neurally-induced contraction appears to be due to elimination of NO produced by non-adrenergic, non-cholinergic vasodilator nerve activation.