Blockade of nitric oxide (NO) synthesis enhances contractile responses to transmural nerve stimulation in guinea-pig pulmonary artery, indicating neuromodulation by endogenous nitric oxide. In the present study, neuromodulatory effects of exogenous NO were examined in guinea-pig pulmonary artery and vas deferens. Application of NO as acid nitrite, to the guinea-pig pulmonary artery, inhibited the contractile response to transmural nerve stimulation as well as contractions to exogenous noradrenaline. The inhibition occurred in a dose-dependent manner. Acid nitrite did not affect stimulation-induced release of [3H]noradrenaline in guinea-pig pulmonary artery. In the guinea-pig vas deferens, contractile 'twitch' responses to brief (25 pulses) transmural nerve stimulation and stimulation-induced release of [3H]noradrenaline was unaffected by acid nitrite. However, 'twitch' responses to prolonged stimulation were inhibited by acid nitrite, and tonic 'hump' responses were either enhanced or unaffected by acid nitrite. In conclusion, exogenous nitric oxide exerted an inhibition of adrenergic neurotransmission post-junctionally in guinea-pig pulmonary artery. In guinea-pig vas deferens, exogenous nitric oxide affected adrenergic and/or non-adrenergic noncholinergic neurotransmission in a complex fashion, however without alteration in noradrenaline release. The data support a role for NO in modulation of neuroeffector transmission, especially by modulation of effector sensitivity, whereas modulation of noradrenaline release seems an unlikely role for NO in these and similar peripheral tissues.
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