title: Angiotensin retains sodium by dephosphorylating mineralocorticoid receptors in renal intercalated cells.
abstract: In this issue of Cell Metabolism, Shibata et al. (2013) show that in renal intercalated cells mineralocorticoid receptors phosphorylated on serine 843 are rendered active by angiotensin-induced dephosphorylation. This finding represents a novel mechanism for regulating nuclear receptor activity, and explains the balance between Na-Cl reabsorption in response to volume depletion and K(+) excretion in response to potassium loading.
authors.affiliation: Prince Henry's Institute, P.O. Box 5152, Clayton, VIC 3168, Australia. Electronic address: john.funder@princehenrys.org.
authors.forename: John W
authors.initials: JW
authors.lastname: Funder
mesh_terms: D000818:Animals; D006801:Humans; D006947:Hyperkalemia / Q000378:metabolism* / Q000503:physiopathology*; D007668:Kidney / Q000378:metabolism* / Q000503:physiopathology*; D018161:Receptors, Mineralocorticoid / Q000378:metabolism*
chemical_list: D018161:Receptors, Mineralocorticoid