Published online Jan 15, 2003. doi: 10.3748/wjg.v9.i1.129
Revised: September 23, 2002
Accepted: October 21, 2002
Published online: January 15, 2003
AIM: To investigate the intragastric mechanisms for regulation of gastric neuroendocrine functions during gastric distention in isolated vascularly perfused rat stomach.
METHODS: Isolated vascularly perfused rat stomach was prepared, then the gastric lumen was distended with either 5, 10 or 15 mL pH7 isotonic saline during a period of 20 min. During the distention, the axonal blocker tetrodotoxin (TTX), the cholinergic antagonist atropine, or the putative somatostatin-antagonist cyclo [7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)] were applied by vascular perfusion. The releases of gastrin and somatostatin were then examined by radioimmunoassay.
RESULTS: The graded gastric distention caused a significant volume-dependent decrease in gastrin secretion [-183 ± 75 (5 mL), -385 ± 86 (10 mL) and -440 ± 85 (15 mL) pg/20 min] and a significant increase of somatostatin secretion [260 ± 102 (5 mL), 608 ± 148 (10 mL) and 943 ± 316 (15 mL) pg/20 min]. In response to 10 mL distention, the infusion of either axonal blocker TTX (10-6 M) or cholinergic blocker atropine (10-7 M) had a similar affect. They both attenuated the decrease of gastrin release by approximately 50%, and attenuated the increase of somatostatin release by approximately 40%. The infusion of somatostatin-antagonist cyclo [7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)] (10-6 M) attenuated the decrease of gastrin release by about 60%. Furthermore, combined infusion of the somatostatin-antagonist and atropine completely abolished distention-induced inhibition of gastrin release.
CONCLUSION: The present data suggest that distention of isolated rat stomach stimulates somatostatin release via cholinergic and non-cholinergic TTX-insensitive pathways. Both somatostatin and intrinsic cholinergic pathways are responsible for distention-induced inhibition of gastrin release.