The Janus effect: two faces of aldosterone.
Inhibition of the nitric oxide pathway by N(omega)-nitro-l-arginine methyl ester (l-NAME) is well known to produce hypertension and proteinuria, but the mechanisms are less straightforward. Prolonged administration of mineralocorticoids mimics the pathological findings produced by l-NAME. Ikeda and colleagues provide a clue to the mechanism by showing that exposure to l-NAME increases plasma aldosterone 50-fold, and that spironolactone markedly attenuates the renal changes. Thus, chronic l-NAME exposure may turn out to be a model of mineralocorticoid excess.
Brem
Andrew S
AS
Division of Kidney Diseases and Hypertension, Rhode Island Hospital, Providence, Rhode Island 02903, USA. Andrew_Brem@Brown.edu
D000305:Adrenal Cortex Hormones / Q000494:pharmacology; D000450:Aldosterone / Q000819:agonists* / Q000097:blood / Q000502:physiology*; D000818:Animals; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013148:Spironolactone / Q000494:pharmacology
D000305:Adrenal Cortex Hormones; D013148:Spironolactone; D000450:Aldosterone; D012964:Sodium; D019331:NG-Nitroarginine Methyl Ester