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Somatostatin secretion was investigated from rodent antral mucosal biopsies maintained in organ culture. Under control conditions, the somatostatin secretory output was fairly constant, with each biopsy releasing a mean value of 29.1 +/- 7.5 pg of hormone over a 15-min period. Incubation of the mucosa in medium containing 5% peptone directly induced a 20-fold increase in medium somatostatin levels to 622.5 +/- 15.5 pg/ml. In contrast, a peptone dialysate was a weaker stimulant of hormone release, inducing a three- to fourfold increase in medium somatostatin concentration. Additionally, it was determined that a peptic hydrolysate of bovine serum albumin was a significantly more potent in vitro stimulant of somatostatin secretion than the intact undigested molecule. These results suggest that the amino acid and peptide constituents of these proteinaceous substances are the major stimulants of somatostatin release in vitro. It is presently uncertain whether this direct peptone-induced release of somatostatin from antral mucosal explants can account for the previously reported [Am. J. Physiol. 235 (Endocrinol. Metab. Gastrointest. Physiol. 4): E410-E415, 1978] gastrin secretory "off response" to the same agent, because addition of exogenous somatostatin to the medium failed to block this peptone-induced gastrin secretory response.

Ahstract. A fraction of isolated and enriched rodent, gastrin-containing G cells was prepared using a previously described technique (1) and employed to investigate the role of calcium in gastrin release in vitvo. Incubation of the enriched G cells in medium containing low extracellular calcium resulted in a significant, 20-40% increase in basal gastrin release. It was determined that hormone secretion is enhanced when the cells are incubated under basal conditions in medium containing low levels of calcium (0-0.3 mM CaCl,) and inhibited when the extracellular calcium concentration is increased above 2.4 mM. Addition of Verapamil, a drug which prevents calcium entry into isolated cells and accelerates calcium efflux, to the medium at a final concentration of 10 pM, induced a significant 2-2.5 fold increase in gastrin release. Peptone-stimulated gastrin release was not influenced by either Verapamil or incubation of the cells in calcium-free medium. The results suggest that inhibition of calcium influx or acceleration of calcium efflux from the G cell may be a critical step in the initiation of gastrin release.