Role of Ca2+ in bombesin-stimulated release of gastrin and somatostatin from isolated perfused rat stomach

Y. S. Guo, J. C. Thompson, Pomila Singh

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Abstract

The role of calcium (Ca2+) in bombesin (BBS)-stimulated release of gastrin and somtatostatin-like immunoreactivity (SLI) was examined in isolated perfused rat stomachs obtained from male rats fasted overnight. The stomachs were perfused via the celiac artery. BBS (1 nM) was perfused alone for 10 min or in combination with various Ca2+ antagonists, including 1) different doses of divalent cationic Ca2+ chelator (EGTA), 2) Ca2+ channel blockers (nifedipine, verapamil), and 3) calmodulin (Ca2+ binding protein) antagonist [trifluoperazine (TFP)]. The effluent was collected for measurement of gastrin and SLI. EGTA at doses of 2 or 5 mM blocked the BBS-mediated release of both gastrin and SLI. After removal of a low dose of EGTA from the perfusate, the release of both gastrin and SLI rebounded. On removal of a high dose of EGTA, however, SLI release remained depressed, but gastrin rebounded even more significantly. In the absence of BBS, the rebound of gastrin release was less dramatic, indicating that reexposure to Ca2+ partially contributed to the rebound phenomenon. Nifedipine (0.1-10 μM) markedly decreased BBS-stimulated release of gastrin and SLI in a dose-dependent fashion; the inhibitory effect of nifedipine on SLI release was significantly stronger than on gastrin release. Verapamil (10 μM) depressed BBS-induced SLI release but not gastrin release. TFP (50 or 100 μM) also resulted in inhibition of bombesin-elicited release of gastrin and SLI in a dose-related manner. These results suggest that BBS stimulation of gastrin and SLI release is dependent on both the availability of extracellular Ca2+ and on an adequate supply of intracellular Ca2+ in the presence of the Ca2+ binding protein, calmodulin. It also became clear that the SLI release induced by BBS was significantly more sensitive to Ca2+ channel blockers than was the release of gastrin in the perfused isolated rat stomach.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume255
Issue number5
StatePublished - 1988

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Bombesin
Gastrins
Somatostatin
Stomach
Egtazic Acid
Calmodulin-Binding Proteins
Trifluoperazine
Nifedipine
Verapamil
Celiac Artery
Chelating Agents

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology

Cite this

@article{b06283ab7bd84b288ea3797fc855dc6a,
title = "Role of Ca2+ in bombesin-stimulated release of gastrin and somatostatin from isolated perfused rat stomach",
abstract = "The role of calcium (Ca2+) in bombesin (BBS)-stimulated release of gastrin and somtatostatin-like immunoreactivity (SLI) was examined in isolated perfused rat stomachs obtained from male rats fasted overnight. The stomachs were perfused via the celiac artery. BBS (1 nM) was perfused alone for 10 min or in combination with various Ca2+ antagonists, including 1) different doses of divalent cationic Ca2+ chelator (EGTA), 2) Ca2+ channel blockers (nifedipine, verapamil), and 3) calmodulin (Ca2+ binding protein) antagonist [trifluoperazine (TFP)]. The effluent was collected for measurement of gastrin and SLI. EGTA at doses of 2 or 5 mM blocked the BBS-mediated release of both gastrin and SLI. After removal of a low dose of EGTA from the perfusate, the release of both gastrin and SLI rebounded. On removal of a high dose of EGTA, however, SLI release remained depressed, but gastrin rebounded even more significantly. In the absence of BBS, the rebound of gastrin release was less dramatic, indicating that reexposure to Ca2+ partially contributed to the rebound phenomenon. Nifedipine (0.1-10 μM) markedly decreased BBS-stimulated release of gastrin and SLI in a dose-dependent fashion; the inhibitory effect of nifedipine on SLI release was significantly stronger than on gastrin release. Verapamil (10 μM) depressed BBS-induced SLI release but not gastrin release. TFP (50 or 100 μM) also resulted in inhibition of bombesin-elicited release of gastrin and SLI in a dose-related manner. These results suggest that BBS stimulation of gastrin and SLI release is dependent on both the availability of extracellular Ca2+ and on an adequate supply of intracellular Ca2+ in the presence of the Ca2+ binding protein, calmodulin. It also became clear that the SLI release induced by BBS was significantly more sensitive to Ca2+ channel blockers than was the release of gastrin in the perfused isolated rat stomach.",
author = "Guo, {Y. S.} and Thompson, {J. C.} and Pomila Singh",
year = "1988",
language = "English (US)",
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journal = "American Journal of Physiology - Endocrinology and Metabolism",
issn = "0193-1849",
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T1 - Role of Ca2+ in bombesin-stimulated release of gastrin and somatostatin from isolated perfused rat stomach

AU - Guo, Y. S.

AU - Thompson, J. C.

AU - Singh, Pomila

PY - 1988

Y1 - 1988

N2 - The role of calcium (Ca2+) in bombesin (BBS)-stimulated release of gastrin and somtatostatin-like immunoreactivity (SLI) was examined in isolated perfused rat stomachs obtained from male rats fasted overnight. The stomachs were perfused via the celiac artery. BBS (1 nM) was perfused alone for 10 min or in combination with various Ca2+ antagonists, including 1) different doses of divalent cationic Ca2+ chelator (EGTA), 2) Ca2+ channel blockers (nifedipine, verapamil), and 3) calmodulin (Ca2+ binding protein) antagonist [trifluoperazine (TFP)]. The effluent was collected for measurement of gastrin and SLI. EGTA at doses of 2 or 5 mM blocked the BBS-mediated release of both gastrin and SLI. After removal of a low dose of EGTA from the perfusate, the release of both gastrin and SLI rebounded. On removal of a high dose of EGTA, however, SLI release remained depressed, but gastrin rebounded even more significantly. In the absence of BBS, the rebound of gastrin release was less dramatic, indicating that reexposure to Ca2+ partially contributed to the rebound phenomenon. Nifedipine (0.1-10 μM) markedly decreased BBS-stimulated release of gastrin and SLI in a dose-dependent fashion; the inhibitory effect of nifedipine on SLI release was significantly stronger than on gastrin release. Verapamil (10 μM) depressed BBS-induced SLI release but not gastrin release. TFP (50 or 100 μM) also resulted in inhibition of bombesin-elicited release of gastrin and SLI in a dose-related manner. These results suggest that BBS stimulation of gastrin and SLI release is dependent on both the availability of extracellular Ca2+ and on an adequate supply of intracellular Ca2+ in the presence of the Ca2+ binding protein, calmodulin. It also became clear that the SLI release induced by BBS was significantly more sensitive to Ca2+ channel blockers than was the release of gastrin in the perfused isolated rat stomach.

AB - The role of calcium (Ca2+) in bombesin (BBS)-stimulated release of gastrin and somtatostatin-like immunoreactivity (SLI) was examined in isolated perfused rat stomachs obtained from male rats fasted overnight. The stomachs were perfused via the celiac artery. BBS (1 nM) was perfused alone for 10 min or in combination with various Ca2+ antagonists, including 1) different doses of divalent cationic Ca2+ chelator (EGTA), 2) Ca2+ channel blockers (nifedipine, verapamil), and 3) calmodulin (Ca2+ binding protein) antagonist [trifluoperazine (TFP)]. The effluent was collected for measurement of gastrin and SLI. EGTA at doses of 2 or 5 mM blocked the BBS-mediated release of both gastrin and SLI. After removal of a low dose of EGTA from the perfusate, the release of both gastrin and SLI rebounded. On removal of a high dose of EGTA, however, SLI release remained depressed, but gastrin rebounded even more significantly. In the absence of BBS, the rebound of gastrin release was less dramatic, indicating that reexposure to Ca2+ partially contributed to the rebound phenomenon. Nifedipine (0.1-10 μM) markedly decreased BBS-stimulated release of gastrin and SLI in a dose-dependent fashion; the inhibitory effect of nifedipine on SLI release was significantly stronger than on gastrin release. Verapamil (10 μM) depressed BBS-induced SLI release but not gastrin release. TFP (50 or 100 μM) also resulted in inhibition of bombesin-elicited release of gastrin and SLI in a dose-related manner. These results suggest that BBS stimulation of gastrin and SLI release is dependent on both the availability of extracellular Ca2+ and on an adequate supply of intracellular Ca2+ in the presence of the Ca2+ binding protein, calmodulin. It also became clear that the SLI release induced by BBS was significantly more sensitive to Ca2+ channel blockers than was the release of gastrin in the perfused isolated rat stomach.

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