| Autor: |
Martinez, V., Curi, A.P., Torkian, B., Schaeffer, J.M., Wilkinson, H.A., Walsh, J.H., Tache, Y. |
| Zdroj: |
Gastroenterology; April 1998, Vol. 114 Issue: 6 p1125-1132, 8p |
| Abstrakt: |
Background & Aims: Somatostatin receptor subtype 2 (sst"2) agonists inhibit gastric secretion. The role of sst"2 in the regulation of acid secretion was assessed using sst"2 knockout mice and urethane to induce somatostatin release. Methods: Acid secretion was monitored every 10 minutes by gastric perfusion and backtitration of perfusates in fasted, urethane-anesthetized C57/129 sst"2 (-/-) mice and wild-type (+/+) mice. The ileal vein was cannulated for drug injection. Intragastric pH and serum gastrin were monitored 1 hour after anesthesia without perfusion. Results: Gastric pH values were lower in sst"2 (-/-) mice (3.8 +/- 0.3) than in wild-type mice (7.1 +/- 0.1, P < 0.05), and there was no difference in gastrin levels. Basal acid output per 2 hours was 10-fold higher in sst"2 knockout mice compared with wild-type mice. The gastrin antibody abolished the high basal acid secretion in sst"2 (-/-) mice and had no effect in wild-type mice. The somatostatin antibody increased basal secretion by 4-fold in wild-type and had no effect in knockout mice. Somatostatin 14 or the sst"2 agonist DC 32-87 inhibited pentagastrin-stimulated acid secretion in wild-type mice, but did not alter basal secretion in knockout mice. Conclusions: These results indicate that sst"2 is the main subtype whereby endogenous somatostatin suppresses gastric acid secretion through inhibition of gastrin action. GASTROENTEROLOGY 1998;114:1125-1132 |
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