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.
Toda
N
N
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
Yoshida
K
K
Okamura
T
T
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology; D004285:Dogs; D004558:Electric Stimulation; D066298:In Vitro Techniques; D009569:Nitric Oxide / Q000378:metabolism; D019335:Nitroarginine; D009638:Norepinephrine / Q000502:physiology*; D010646:Phentolamine / Q000494:pharmacology; D013699:Temporal Arteries / Q000187:drug effects* / Q000294:innervation; D013779:Tetrodotoxin / Q000494:pharmacology; D014316:Tritium; D014662:Vasoconstrictor Agents
D014662:Vasoconstrictor Agents; D014316:Tritium; D019335:Nitroarginine; D009569:Nitric Oxide; D013779:Tetrodotoxin; D001120:Arginine; D009638:Norepinephrine; D010646:Phentolamine