Effects of sodium depletion on plasma renin activity and on the urinary excretion of cyclic AMP and aldosterone in hypoparathyroid patients.
The effect of sodium depletion on plasma renin activity (PRA), urinary cyclic AMP and urinary aldosterone excretion was studied in hypoparathyroid patients whose basal urinary cylic AMP excretion (urinary cAMP) was less than 50% of that observed in normal subjects. During 7 days of sodium depletion, PRA, urinary aldosterone and urinary cAMP each rose significantly. Administration of the beta-blocker propranolol, 160 mg/day, during 5 further days of sodium depletion produced a fall in PRA and urinary cAMP, but no change in urinary aldosterone excretion. The dissociation in these effects suggests that the increase in aldosterone secretion during sodium depletion may be mediated by pathways other than the renin-angiotensin and adenyl cyclase systems. There was a high degree of correlation between PRA and urinary cAMP (P less than 0.001) during the period of sodium depletion, but not significant relationship between these parameters was found during control and propranolol phases, or in control studies in normal subjects. These findings suggest that beta-adrenergic receptors have a role in mediating the effects of sodium depletion upon renin secretion and adenyl cyclase activity.
D000328:Adult; D000450:Aldosterone / Q000652:urine*; D002118:Calcium / Q000097:blood; D000242:Cyclic AMP / Q000652:urine*; D004032:Diet; D006801:Humans; D007011:Hypoparathyroidism / Q000378:metabolism*; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000627:therapeutic use; D011433:Propranolol / Q000494:pharmacology; D012083:Renin / Q000097:blood*; D012964:Sodium / Q000097:blood / Q000494:pharmacology*
D010281:Parathyroid Hormone; D000450:Aldosterone; D012964:Sodium; D011433:Propranolol; D000242:Cyclic AMP; D012083:Renin; D002118:Calcium