Role of angiotensin II in the pathogenesis of hyperdipsia in chronic renal failure.
The relation of thirst to the renin-angiotensin system was examined in 38 patients with chronic renal failure receiving hemodialysis treatment. They were classified into three groups, ie, group 1 (19 patients), no or modest thirst; group 2 (13 patients), moderate thirst; and group 3 (six patients), excessive thirst. The plasma renin activity, plasma angiotensin II levels, and interdialytic weight gains of groups 1 to 3 significantly increased in a progressive manner with intensity of thirst. The hyperdipsia experienced by four patients in group 3 ameliorated after administration of an angiotensin-converting-enzyme inhibitor. The hyperdipsia of some patients with chronic renal failure therefore appears to be mediated by increased production of endogenous angiotensin II.
D000328:Adult; D000368:Aged; D000804:Angiotensin II / Q000097:blood / Q000502:physiology*; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D002216:Captopril / Q000627:therapeutic use; D004326:Drinking; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D012083:Renin / Q000097:blood; D013894:Thirst / Q000187:drug effects / Q000502:physiology*
D001786:Blood Glucose; D000804:Angiotensin II; D002216:Captopril; D012083:Renin