Angiotensin retains sodium by dephosphorylating mineralocorticoid receptors in renal intercalated cells.

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.