The role of NO in the contractility of rabbit small intestine in vitro: effect of K+ channels.

Nitric oxide (NO) is an inhibitory neurotransmitter of intestinal smooth muscle cells. The aim of this study was to determine the role of NO in the contractility of rabbit small intestine smooth muscle in vitro. The amplitude, frequency and tone of spontaneous contractions in longitudinal and circular smooth muscle of duodenum, jejunum and ileum were determined and the sodium nitroprusside (SNP), acetylcholine (ACh) and KCl responses were quantified. L-NAME, L-NNA, L-arginine and D-arginine did not affect the amplitude, frequency and tone of spontaneous contractions. ODQ (10(-6) M) increased the tone of spontaneous contractions of the types of tissues examined, and the amplitude in ileum, without modifying the frequency. SNP (10(-4) M) evoked relaxations that were not influenced by atropine (10(-6) M) plus guanethidine (10(-6) M), apamin (10(-8) M) or glybenclamide (10(-6) M), but were increased by TTX (10(-6) M) and verapamil (10(-7) M). SNP-induced relaxations were reduced by charybdotoxin (10(-8) M) and ODQ (10(-6) M). ODQ (10(-5) M) reduced ACh-induced contractions, but it did not influence KCl-evoked contractions. Those results suggest that NO modulates the spontaneous contractions of small intestine in rabbits. This effect is mediated by cGMP and Ca2+-dependent K+ channels of large conductance.