Role of nitric oxide from the endothelium on the neurogenic contractile responses of rabbit pulmonary artery

The effects of L-N G-nitro arginine (L-NO 2Arg), a stereospecific inhibitor of nitric oxide formation, on the responsiveness of rabbit pulmonary artery to transmural electrical stimulation were studied. The contractile response evoked by electrical stimulation at 4 Hz was abolished by tetrodotoxin (10 −7 M) and depressed to approximately 10% by bunazosin (10 -6 M), an α 1-antagonist. Pretreatment with (L-NO 2Arg) (10 −5 M) significantly potentiated the response to electrical stimulation without changing the resting tension. D-NO 2Arg (10 −5 M) did not show such a potentiating action. In endothelium-denuded arteries, (L-NO 2Arg), did not potentiate the response to electrical stimulation. The effect of (L-NO 2Arg) on endogenous noradrenaline release in response to electrical stimulation was also examined by HPLC with electrochemical detection; (L-NO 2Arg) did not affect noradrenaline release. The contractions induced by exogenous noradrenaline (10 −6-10 −5 M) were enhanced by L-NO 2Arg, but not by D-NO 2Arg. These results suggest that the vasoconstriction induced by sympathetic nerve stimulation in the rabbit pulmonary artery is modulated by endogenous nitric oxide or nitric oxide-like substances released from endothelial cells.