Impaired 11 beta-hydroxysteroid dehydrogenase contributes to renal sodium avidity in cirrhosis: hypothesis or fact?
Exaggerated renal sodium retention with concomitant potassium loss is a hallmark of cirrhosis and contributes to the accumulation of fluid as ascites, pleural effusion, or edema. This apparent mineralocorticoid effect is only partially explained by increased aldosterone concentrations. I present evidence supporting the hypothesis that cortisol confers mineralocorticoid action in cirrhosis. The underlying molecular pathology for this mineralocorticoid receptor (MR) activation by cortisol is a reduced activity of the 11 beta-hydroxysteroid dehydrogenase type 2, an enzyme protecting the MR from promiscuous activation by cortisol in healthy mammalians.
Frey
Felix J
FJ
Department of Nephrology and Hypertension, Inselspital, University of Berne, Switzerland. felix.frey@insel.ch
D042842:11-beta-Hydroxysteroid Dehydrogenases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism; D008103:Liver Cirrhosis / Q000378:metabolism*; D011188:Potassium / Q000097:blood; D051381:Rats; D018161:Receptors, Mineralocorticoid / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*
D001647:Bile Acids and Salts; D018161:Receptors, Mineralocorticoid; D012964:Sodium; D042842:11-beta-Hydroxysteroid Dehydrogenases; D011188:Potassium; D006854:Hydrocortisone