Modulation of neuroeffector transmission in the guinea pig pulmonary artery by endogenous nitric oxide.

The influence of endogenous nitric oxide (NO) on neuroeffector transmission in segments of guinea pig pulmonary artery was analyzed by application of NG-monomethyl-L-arginine (L-NMMA). L-NMMA enhanced contractile responses to nerve stimulation and this enhancement was counteracted by L-arginine. The enhancement remained after removal of the endothelium. L-NMMA enhanced contractions to exogenous noradrenaline. After blockade of adrenergic transmission by phentolamine, L-NMMA enhanced contractions induced by nonadrenergic-noncholinergic (NANC) neurotransmission. Stimulation-induced release of [3H]noradrenaline was unchanged by L-NMMA. The results suggest that endogenous NO exerts a postjunctional inhibition on adrenergic neurotransmission in the guinea pig pulmonary artery. A concomitant pre- and/or postjunctional inhibition of NANC transmission is implicated. The neuromodulation by NO does not require an intact endothelium.