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Gastroenterology. 1998 Jun;114(6):1125-32.

High basal gastric acid secretion in somatostatin receptor subtype 2 knockout mice.

Author information

1
CURE: Digestive Diseases Research Center, Veterans Administration Medical Center West Los Angeles, USA. vmartine@ceu.upv.es

Abstract

BACKGROUND & AIMS:

Somatostatin receptor subtype 2 (sst2) agonists inhibit gastric secretion. The role of sst2 in the regulation of acid secretion was assessed using sst2 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 sst2 (-/-) 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 sst2 (-/-) 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 sst2 knockout mice compared with wild-type mice. The gastrin antibody abolished the high basal acid secretion in sst2 (-/-) 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 sst2 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 sst2 is the main subtype whereby endogenous somatostatin suppresses gastric acid secretion through inhibition of gastrin action.

PMID:
9609748
DOI:
10.1016/s0016-5085(98)70417-2
[Indexed for MEDLINE]

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