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Role of Aldosterone and SGK1 in ENaC Expression

, : Role of Aldosterone and SGK1 in ENaC Expression. FASEB Journal 18(4-5): Abst 681 10

Epithelial sodium channels (ENaC) play a critical role in the regulation of sodium balance in the body. Depending on the physiological condition, ENaC subunits can form channels with small (4-6 pS) conductances and larger (25-30 pS) conductances which are highly selective (HSC) and nonselective (NSC) for sodium, respectively. Aldosterone, a steroid hormone, plays a critical role in the regulation of ENaC. In the presence of aldosterone, there is an increase in the number of HSC compared to NSC channels. Aldosterone does not change ENaC message levels in transfected cells, but in the presence of aldosterone the ratio of HSC to NSC channels in cell-attached patches significantly increases compared to aldosterone free cells. It is also known that aldosterone upregulates SGK1, (serum and glucocorticoid dependent kinase) which also has an effect on ENaC but the mechanism is unclear. Understanding the pathway through which SGK1 affects the expression of the type of ENaC in the membrane is the focus of this study. To examine the role of SGK1 on ENaC, alpha, beta, and gamma xENaC subunits were expressed in CHO cells in the presence or absence of aldosterone. Our results show that in the absence of SGK1 and aldosterone, the predominant channel expressed is a NSC channel with a conductance of 27 pS. However, in the presence of SGK1, even in the continued absence of aldosterone, a lower conductance channel, ~7 pS, consistently appears in the patch. Our data suggest that SGK1 mimics the effect of aldosterone by increasing the number of HSC compared to NSC channels that are present in the membrane. Supported by DK37963.


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