AJP - Gastrointestinal and Liver Physiology, Vol 255, Issue 5 627-G632, Copyright © 1988 by American Physiological Society
Role of Ca2+ in bombesin-stimulated release of gastrin and somatostatin from isolated perfused rat stomach
Y. S. Guo, J. C. Thompson and P. Singh
Department of Surgery, University of Texas Medical Branch, Galveston 77550.
The role of calcium (Ca2+) in bombesin (BBS)-stimulated release of gastrin
and somatostatin-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
microM) 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 microM)
depressed BBS-induced SLI release but not gastrin release. TFP (50 or 100
microM) also resulted in inhibition of bombesin-elicited release of gastrin
and SLI in a dose-related manner.(ABSTRACT TRUNCATED AT 250 WORDS)
