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Review
. 2015 Nov 1;309(9):R1068-70.
doi: 10.1152/ajpregu.00135.2015. Epub 2015 Jul 1.

Renal mineralocorticoid receptor and electrolyte homeostasis

Andrew S Terker  1 , David H Ellison  2
Affiliations
Review

Renal mineralocorticoid receptor and electrolyte homeostasis

Andrew S Terker et al. Am J Physiol Regul Integr Comp Physiol. .

Abstract

The renal mineralocorticoid receptor (MR) is a steroid hormone receptor essential for maintaining electrolyte homeostasis. Its role in mediating effects of aldosterone was likely vital in enabling the evolution of terrestrial life. Dysregulated aldosterone-MR signaling has been identified as the cause of multiple clinical diseases, suggesting the physiological importance of the MR. While the physiology of this pathway has been studied for over 60 years, only more recently have genetic mouse models been available to dissect its function in vivo. This review will focus on recent advances in our knowledge of MR function with an emphasis on these models.

Keywords: Na+ Cl− cotransporter; homeostasis; mineralocorticoid; potassium; sodium.

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Figures

Fig. 1.
Fig. 1.
Model of how aldosterone affects Na+ Cl− cotransporter (NCC) in (pseudo-) hyperaldosterone states. Canonical aldosterone signaling increases epithelial Na+ channel (ENaC)-mediated Na+ reabsorption along the connecting tubule (CNT)-collecting duct (CD) (CNT/CD), driving electrogenic K+ secretion, which reduces plasma [K+]. Plasma [K+] secondarily signals NCC in the distal convoluted tubule (DCT) via altered membrane potential and intracellular [Cl−] (not shown). Opposite effects would occur to suppress NCC activity in (pseudo-) hypoaldosterone states.
See this image and copyright information in PMC

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