Elevated serum gastrin after food intake or acid blockade evokes hypocalcemia.

Gastrin lowers blood Ca2+ in the rat. Recently, it was suggested that gastrin causes hypocalcemia by releasing gastrocalcin, a hypothetical peptide hormone thought to reside in the acid-producing part of the stomach. The results of the present study suggest that not only exogenous gastrin but also gastrin of endogenous origin lowers blood Ca2+. Food intake in fasted intact rats produced a transient drop in blood Ca2+, probably induced by the postprandial rise in serum gastrin. Food intake in fasted gastrectomized or fundectomized (acid-producing part extirpated) rats failed to induce any lowering of the blood Ca2+, supporting the view that the gastrin-evoked hypocalcemia is dependent upon a factor in the oxyntic mucosa. Also, the increase in serum gastrin concentration following intraperitoneal injection of the histamine H2-receptor antagonist ranitidine was associated with a drop in blood Ca2+ and also the ranitidine-evoked hypocalcemia could be prevented by gastrectomy. We suggest that endogenous gastrin evokes hypocalcemia by the same mechanism as exogenous gastrin, i.e., by mobilization of gastrocalcin from the acid-producing part of the stomach.