Inhibitory neural pathway regulating gastric emptying in rats.

The relaxation of the pylorus is one of the most important factors for promoting gastric emptying. However, the role of inhibitory neurotransmitters in the regulation of pyloric relaxation and gastric emptying remains unclear. In this study, we investigated the effects of NO biosynthesis inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), and calcium dependent potassium channel blocker, apamin, on vagal stimulation-induced pyloric relaxation and gastric emptying in rats. Sodium nitroprusside (SNP), adenosine 5'-triphosphate (ATP), vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating peptide (PACAP) caused pyloric relaxations in a dose dependent manner in vivo. Apamin (120 microg/kg) significantly reduced ATP and PACAP-induced pyloric relaxations without affecting SNP- or VIP-induced relaxations. Vagal stimulation (10 V, 1 ms, 1-20 Hz)-induced pyloric relaxation was significantly inhibited by L-NAME (10 mg/kg). The combined administration of L-NAME and apamin almost completely abolished vagal stimulation-induced pyloric relaxation. L-NAME and apamin significantly increased spontaneous contractions in the antrum, pylorus and duodenum. Increased motility index by L-NAME and apamin was significantly higher in the pylorus and duodenum, compared to that of antrum. L-NAME and apamin significantly delayed liquid gastric emptying. These results suggest that besides NO, probably ATP and PACAP, act as inhibitory neurotransmitters in the rat pylorus and regulate gastric emptying.