Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 2004 Dec;370(6):510-20.
doi: 10.1007/s00210-004-0992-8. Epub 2004 Nov 20.

Role of somatostatin receptors on gastric acid secretion in wild-type and somatostatin receptor type 2 knockout mice

Affiliations
Comparative Study

Role of somatostatin receptors on gastric acid secretion in wild-type and somatostatin receptor type 2 knockout mice

Laura Piqueras et al. Naunyn Schmiedebergs Arch Pharmacol. 2004 Dec.

Abstract

Somatostatin, probably acting through somatostatin type 2 receptors (SSTR2), is the main inhibitor of gastric acid secretion. We characterized gastric acid secretion in SSTR2 knockout mice, and used preferential somatostatin receptor agonists to assess the relative role of SSTR1, 2, 3, 4, and 5 on gastric acid secretion. Basal gastric acid secretion and the secretory response to a meal were similar in conscious wild-type and knockout mice. However, under urethane anesthesia, which releases endogenous somatostatin, SSTR2 knockout mice had a basal secretion 11-15-fold higher than wild-type animals (micromol/10 min:1.40+/-0.09 vs. 0.10+/-0.01, p<0.05). Gastrin immunoneutralization or H(2) receptors blockade (cimetidine), but not cholinergic blockade (atropine), reduced the high basal secretion in SSTR2 knockout mice. In SSTR2 knockout mice, gastrin and histamine stimulated acid secretion with similar efficacy, while in wild-type mice histamine was more effective than gastrin. SSTR2 knockout mice showed also a hypersecretory response to pylorus ligation compared with wild-type animals. In wild-type mice, somatostatin-14, SMS 201-995, and the SSTR2-preferential agonist, DC 32-87, inhibited gastrin-stimulated acid secretion with an order of potency SMS 201-995>DC 32-87>somatostatin-14. Preferential agonists for the SSTR1, 3, 4, and 5 were devoid of any effect. None of the compounds tested affected the high basal secretion observed under urethane anesthesia in SSTR2 knockout mice. These results show that gastric antisecretory effects of peripheral somatostatin are mediated solely through SSTR2. In the absence of functional SSTR2 other somatostatin receptors do not compensate for the lack somatostatin-SSTR2-mediated inhibition. Basal acid secretion and the response to a meal are normal in conscious SSTR2 knockout mice, suggesting the presence of somatostatin-independent mechanisms that compensate for the lack of somatostatin-SSTR2-mediated inhibitory responses.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Peptides. 1995;16(7):1257-62 - PubMed
    1. Am J Physiol. 1995 Jan;268(1 Pt 1):G102-6 - PubMed
    1. Eur J Pharmacol. 2002 Oct 4;452(2):235-43 - PubMed
    1. Gastroenterology. 1989 Dec;97(6):1406-13 - PubMed
    1. Am J Physiol. 1997 Jun;272(6 Pt 1):G1481-8 - PubMed

Publication types

LinkOut - more resources