Effect of parathyroid hormone on plasma renin activity and sodium excretion.
The interaction between parathyroid hormone (PTH) and the renin-angiotensin system was evaluated in pentobarbital-anesthetized dogs. An intravenous infusion of bovine PTH (1-34) for 1 h was accompanied by a 57% increase (13.7-21.6 ng/ml per h) in plasma renin activity (PRA) which returned toward control levels during the recovery period. Sodium and phosphate excretion also increased. Second the endogenous secretion of PTH was stimulated by infusion of citrate into the blood supply of the thyroparathyroid glands to determine if the stimulatory effect on renin occurred with endogenous secretion of PTH. Phosphate excretion increased, which confirmed PTH secretion. There was a significant rise (57%) in both PRA (6.1-9.8 ng/ml per h) and sodium excretion, the magnitude of the sodium response modulating the increase in PRA. Blood pressure remained constant. In a third set of experiments, thyrocalcitonin was infused intravenously and had no effect on PRA. These data indicate that both exogenous and endogenous PTH can elevate PRA and increase sodium excretion. The sodium effect is probably the result of inhibition of proximal sodium reabsorption by PTH. The mechanism by which PTH elevates PRA is not known.
D000818:Animals; D001692:Biological Transport; D002116:Calcitonin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism / Q000652:urine*; D004285:Dogs; D007668:Kidney / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000494:pharmacology*; D012083:Renin / Q000097:blood*; D012964:Sodium / Q000378:metabolism / Q000652:urine
D010281:Parathyroid Hormone; D002116:Calcitonin; D012964:Sodium; D012083:Renin; D002118:Calcium