Investigation of aldosterone action on ENaC in salt-sensitive hypertension

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The present study has clarified the following points.In the salt-sensitive hypertensive Dahl rat, ENaC expression was abnormally increased in high salt diet, but not in the salt-resistant hypertensive Dahl rat.In the salt-sensitive hypertensive Dahl rat, high salt diet abnormally upregulated the expression of SGK1, which regulates the intracellular trafficking of ENaC.These observations suggest that in the salt-sensitive hypertensive Dahl rat, expression of ENaC and its regulator, SGK1, is abnormally regulated by high salt-diet, resulting in hypertension.This abnormally upregulation of ENaC expression was partially diminished by a flavonoid, quercetin. Hyposomotic stress elevated the expression of ENaC.This hyposmotic stress-induced elevation of ENaC expression was mediated via a decrease in the cytosolic chloride ion concentration.Aldosterone inhibited the endocytosis of ENaC protein.The aldosterone-induced ENaC proteins were mainly located in ERp38 was involved in hyposmotic stress-induced upregulation of ENaC expression.