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.

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