Actions of somatostatins on gastric smooth muscle cells

Z. F. Gu, T. Pradhan, D. H. Coy, S. Mantey, N. W. Bunnett, R. T. Jensen, P. N. Maton

Research output: Contribution to journalArticlepeer-review


The effects of somatostatin-28, somatostatin-14, and a synthetic somatostatin octapeptide analogue, D-Phe-Cys-Tyr-D-Trp-Lys-Thr-Cys-Nal-NH2 (cyclo SS-8) were examined on contraction of dispersed gastric smooth muscle cells from guinea pigs. The somatostatins did not cause contraction of gastric smooth muscle cells, nor did they inhibit carbachol-stimulated contraction. However, they reversed vasoactive intestinal peptide (VIP)- induced inhibition (relaxation) of carbachol-stimulated contraction. Somatostatin-28 had a half-maximal effect (EC50) at 1.6 ± 0.8 nM, cyclo SS-8 at 0.6 ± 0.3 nM, but somatostatin-14 had no effect even when used in concentrations as high as 1 μM. Incubation of muscle cells with peptidase inhibitors phosphoramidon (1 μM) plus amastatin (10 μM) had no effect on the EC50 of somatostatin-28 or cyclo SS-8 but increased the potency of somatostatin-14 >1,000-fold. When peptides were incubated with muscle cells and the products applied to high-performance liquid chromatography, cyclo SS- 8 was not degraded, but somatostatin-14 was rapidly degraded when present alone, and the addition of peptidase inhibitors partially inhibited the degradation. Cyclo SS-8 had its maximal effect at 0.5-1 min and inhibited relaxation induced by VIP, isoproterenol, glucagon, or dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP). Cyclo SS-8 partially inhibited the increase in VIP-stimulated cAMP. Preincubation with pertussis toxin blocked the inhibitory action of cyclo SS-8 on VIP or DBcAMP-induced relaxation. These results indicate that gastric smooth muscle cells rapidly degrade somatostatin-14 and suggest that muscle cell peptidases could have a major effect on the actions of somatostatin-14. Furthermore, gastric muscle cells possess somatostatin receptors, occupation of which inhibits relaxation induced by a variety of agents. Somatostatins act both through the guanine nucleotide regulatory protein G(i) to inhibit adenylate cyclase and at sites distal to the generation of cAMP.

Original languageEnglish (US)
Pages (from-to)G432-G438
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number3 25-3
StatePublished - 1992


  • adenosine 3',5'-cyclic monophosphate
  • muscle contraction
  • muscle relaxation
  • regulatory G proteins
  • vasoactive intestinal peptide

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)


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