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AIM:To investigate the intragastric mechanisms forregulation of gastric neuroendocrine functions during gastricdistention in isolated vascularly perfused rat stomach.METHODS:Isolated vascularly perfused rat stomach wasprepared,then the gastric lumen was distended with either5,10 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 putativesomatostatin-antagonist cyclo[7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)]were applied by vascular perfusion.Thereleases of gastrin and somatostatin were then examinedby radioimmunoassay.RESULTS:The graded gastric distention caused a significantvolume-dependent decrease in gastrin secretion[-183±75(5ml),-385±86(10 ml)and -440±85(15 ml)pg/20 min]and asignificant increase of somatostatin secretion[260±102(5 ml),608±148(10 ml)and 943±316(15 ml)pg/20 min].In responseto 10 ml distention,the infusion of either axonal blocker TTX(10~(-6)M)or cholinergic blocker atropine(10~(-7)M)had a similaraffect.They both attenuated the decrease of gastrin releaseby approximately 50%,and attenuated the increase ofsomatostatin release by approximately 40%.The infusion ofsomatostatin-antagonist cyclo[7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)](10~(-6)M)attenuated the decrease of gastrin releaseby about 60%.Furthermore,combined infusion of thesomatostatin-antagonist and atropine completely abolisheddistention-induced inhibition of gastrin release.CONCLUSION:The present data suggest that distention ofisolated rat stomach stimulates somatostatin release viacholinergic and non-cholinergic TTX-insensitive pathways.Bothsomatostatin and intrinsic cholinergic pathways are responsiblefor distention-induced inhibition of gastrin release.
AIM: To investigate the gastric neuroendocrine functions during gastric discharge in vascularly perfused rat stomach. METHODS: Isolated vascular lysed peritoneum gastric was prepared, then the gastric lumen was distended with either 5, 10 or 15 ml pH 7 isotonic saline during a period of 20 min. Drawing 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. Thereleases 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 ) pg / 20 min] and asignificant increase of somatostatin secretion [260 ± 102 (5 ml), 608 ± 148 (10 ml) and 943 ± 316 (15 ml) pg / 20 min] of either axonal blocker TTX (10 ~ (-6) M) or cholinergic blocker atropine (10 ~ (-7) M) had a similaraffect. They both attenuated the decrease of gastrin release by about 50%, and attenuated the increase of somatostatin release by about 40%. The infusion of somatostatin-antagonist cyclo [7-aminoheptanoyl-Phe -F-Lys-Thr (Bzl)] (10 -6 M) attenuated the decrease of gastrin release by about 60%. Fuerthermore, combined infusion of the somatostatin-antagonist and atropine completely abolished disposition-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. Butothmatostatin and intrinsic cholinergic pathways are responsible for distention-induced inhibition of gastrin release.