Angiotensin retains sodium by dephosphorylating mineralocorticoid receptors in renal intercalated cells.
Where this comes from
- Record sourced from PubMed, PMID 24206658.
- Also identified by DOI 10.1016/j.cmet.2013.10.010.
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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.
Medical subject headings
- Hyperkalemia
- Kidney
- Receptors, Mineralocorticoid