NITRIC-OXIDE AS A PUTATIVE NONADRENERGIC, NONCHOLINERGIC NEUROTRANSMITTER IN DOG DUODENAL MUSCLES

We investigated the behavior of nitric oxide (NO) in non-adrenergic, non-cholinergic (NANC) nerve-mediated relaxation in dog duodenal longitudinal muscle in vitro. Transmural electrical stimulation (TES) produced brief contraction followed by weak relaxation of the muscle strip. Atropine eliminated contraciton and significantly potentiated relaxation. Relaxations were markedly suppressed by treatment with N-G-nitro-L-arginine (L-NA), a NO synthase inhibitor, but not by D-enantiomer (D-NA). The suppression by L-NA was reversed by L-arginine, but not by D-arginine. Relaxations induced by TES were eliminated by tetrodotoxin. Neuronal cell bodies and bundles containing NADPH diaphorase, inferred to be identical to NO synthase, were histologically determined in the myenteric plexus of the duodenal muscle. In addition to our earlier study on cerebral arteries, these findings may indicate that NO acts as a neurotransmitter in NANC inhibitory nerves, which contribute to regulation of the muscular tone and motility by counteracting the excitatory cholinergic nerve.