Participation of nitric oxide in the relaxation of the rat gastric corpus.

Abstract

Nitric oxide is an important mediator of the relaxation in the rat gastric fundus. The present study investigates the role of NO in the rat gastric corpus in vitro, since the corpus differs from the fundus with regard to its physiological function and its spontaneous motor behaviour. In the presence of guanethidine electrically induced relaxations of circular, mucosa-free corpus strips precontracted with bethanechol were concentration-dependently reduced by the NO-synthase inhibitors L-NG-nitro-arginine (L-NNA) or L-NG-nitro-arginine-methyl-ester (L-NAME). The D-enantiomers were markedly less active. The inhibitory effect of L-NAME could be prevented by L-arginine. L-NNA and L-NAME, however, did not influence spontaneous motility or the bethanechol-induced contraction. Vasoactive intestinal polypeptide or sodium nitroprusside also relaxed the muscle strips, but these relaxations were not affected by L-NAME. When the corpus strips were stimulated electrically from baseline, they reacted with a contraction followed by relaxation. L-NNA or L-NAME blocked the relaxatory and enhanced the contractile component. In strips that also reacted with a rebound contraction, it was blunted by L-NAME. These effects of the NO-synthase inhibitors were abolished in the presence of atropine. Apamin increased the electrically induced contraction of the muscle strips. Inhibition of the relaxation together with a further shift to contraction could only be seen when apamin was combined with L-NNA. The inhibitory action of apamin and apamin + L-NNA was not influenced by atropine. The results demonstrate a role of NO in the relaxation of the circular muscle of the rat gastric corpus both at a postsynaptic site and via inhibition of acetylcholine release. The relaxation induced by vasoactive intestinal polypeptide does not involve NO.