1. The effect of parathyroid hormone on gastric bicarbonate secretion was determined in the anaesthetized guinea pig. Subcutaneous injections of bovine parathyroid hormone (75 U.S.P units day−1 kg−) for 7 days caused a significant increase in HCO3− output. There was also a rise in K+ output and a slight elevation of H+ secretion. A similar increase in HCO3− output occurred after acute intravenous injection of the hormone (75 U.S.P. units/kg).
2. Both chronic and acute administration of parathyroid hormone caused a significant increase in serum calcium concentration and it is likely that the changes in gastric ion outputs reflect raised calcium levels. Given alone intravenous calcium (1.5 mg/kg body wt.) stimulated gastric secretion of both HCO3− and H+.
3. To determine whether parathyroid hormone had a direct action on gastric ion transport experiments were performed in the amphibian isolated mucosa. Antrum transports HCO3− spontaneously while HCO3− transport in fundus was studied after inhibition of the greater H+ secretion by the histamine H2-receptor antagonist metiamide. Parathyroid hormone at a concentration of 0.2 United States Pharmacopea (U.S.P.) unit/ml in the nutrient-side bathing solution inhibited both antral and fundic HCO3− transport. A higher concentration (2.0 units/ml) had no effect on fundic H+ secretion.
4. The inhibitory effect in vitro was greater in the antrum and parathyroid hormone may almost abolish the active component of HCO3− transport in this tissue. It is likely that any similar inhibition of gastric HCO3− secretion by parathyroid hormone in vivo is masked by the stimulatory effects of released calcium.
