Suppression by N<SUP>G</SUP>-Nitro-L-Arginine of Relaxations Induced by Non-Adrenergic, Non-Cholinergic Nerve Stimulation in Dog Duodenal Longitudinal Muscle

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In dog duodenal longitudinal muscle strips, transmural electrical stimulation (10 Hz, 15 sec) elicited a transient contraction, which was abolished by tetrodotoxin and atropine but potentiated by treatment with N<SUP>G</SUP>-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor. The potentiation was reversed by L-arginine but not by its D-enanthiomer. Acetylcholine-induced contractions were not influenced by L-NA. After treatment with atropine, the electrical neural stimulation relaxed the muscle strips partially contracted with bradykinin, the relaxation being abolished by tetrodotoxin and suppressed by L-, but not D-, NA. L-arginine reversed the L-NA-induced inhibition. Oxyhemoglobin abolished the relaxation caused by nerve stimulation and NO. The neurally-induced relaxation was not attenuated by adrenoceptor antagonists and indomethacin. It is concluded that electrical stimulation of non-adrenergic, non-cholinergic nerves relaxes dog duodenal smooth muscle, due possibly to NO produced upon neural excitation, and potentiation by L-NA of the contractile response to cholinergic nerve stimulation would be derived from elimination of the neurally-induced relaxation.