Whether gastrin plays a role in normal calcium homeostasis remains a controversial question. This gastrointestinal hormone has been implicated as a calcitonin secretagogue from which the hypocalcemic effect subsequently resulted in the pig (1, 2), while other investigators, using the rat, indicated that the hypocalcemic effect of gastrin was direct and independent of calcitonin release (3,4). However, it is an attractive possibility that there could exist a calcium regulatory system involving gastrin acting as a rapid antihypercalcemic agent during the transitory calcium increment due to rapid calcium absorption. It is also known that circulating levels of gastrin increase during hypercalcemia in both man (5) and cat (6).In the work reported here, evidence is presented to suggest that gastrin does indeed cause a hypocalcemic effect independent of calcitonin, and the preliminary search indicates that the effect is due, at least in part, to calcium excretion into the gastrointestinal lumen.
Methods. Measurement of plasma calcium, urinary calcium excretion, bile and gastric calcium secretions.Adult female (Fisher) rats weighing between 200-220 g and maintained on commercial rat pellets, were fasted overnight. After the rat was anesthetized with Nembutal sodium, the femoral artery and vein were cannulated, respectively, for blood samples (0.2 ml) collection and for infusion to maintain body fluid. Urine was collected via a urethra cannula and the body temperature was maintained with a rectal telethermometer probe and temperature regulator (YSI Telethermometer Controller). Porcine gastrin (Sigma Chem. Co.) at a dose of 50 pg/lOO g rat in 0.5 ml or its vehicle (0.9% saline in the case of sham control) was administered intraperitoneally into both intact rats and rats which had been thyroparathyroidectomized (TPTX) by blunt dissection 2 hr previously. The dose used here was phar-40