NITRIC-OXIDE SYNTHASE INHIBITOR INHIBITS CATECHOLAMINES RELEASE CAUSED BY HYPOGASTRIC SYMPATHETIC-NERVE STIMULATION

Recent studies suggest that nitric oxide (NO) plays a significant role in the parasympathetic inhibitory neurotransmission to the internal anal sphincter (IAS). The role of NO in the sympathetic neurotransmission in the gut is not known. The resting intraluminal pressures of anesthetized opossum IAS (IASP) were monitored using low-compliance continuously perfused catheters. The plasma levels of catecholamines norepinephrine, epinephrine and dopamine were measured using a radioenzymatic assay. Parallel studies to determine the effects of hypogastric nerve stimulation (HGNS) on the resting IASP and catecholamine release were performed. The influence of NO in the sympathetic neurotransmission was determined by examining the effect of the NO synthase inhibitor L-N(G)-nitro-arginine (L-NNA) and the reversal of the effect by L-arginine. HGNS caused a frequency-dependent rise in the IASP accompanied by rises in norepinephrine, epinephrine and dopamine levels. The increases in the IASP and norepinephrine, epinephrine and dopamine levels were stereoselectively and significantly attenuated by L-NNA. Furthermore, the L-NNA-induced attenuation of rises in the resting IASP and catecholamine levels in response to HGNS was reversed stereoselectively by L-arginine. These studies for the first time (to the authors' knowledge) show that the NO synthase inhibitor causes specific suppression of sympathetic neurotransmitter release in the gut smooth muscle. It was concluded that, in the anorectum, NO has a facilitory role in the release of sympathetic neurotransmitters.