Abstract
Disturbance of renal Na+ reabsorption develops hypertension in Dahl salt-sensitive (DS) rat. We previously reported that high sodium diet decreased the plasma aldosterone level, evertheless high sodium diet elevated mRNA expression of epithelial Na+ channel (ENaC) and blood pressure in the kidney of DS rat, suggesting that ENaC expression is induced independent of aldosterone. Therefore, we studied whether aldosterone regulates ENaC expression in DS rat. In addition to ENaC expression, we assessed the effect of aldosterone on serum and glucocorticoid-regulated kinase 1 (sgk1) contributing to renal Na+ reabsorption. Aldosterone (1.5 mg/kg B.W.) was subcutaneously injected into adrenalectomized DS and Dahl salt-resistant (DR) rats kept with normal diet and water supplemented with 9 g/l NaCl for 2 weeks after adrenalectomy. RNA was extracted from the kidney 6 h after the injection. In DR rats, aldosterone injection increased expression of alpha-ENaC and sgk1. On the other hand, in DS rats, aldosterone injection elevated expression of alpha-ENaC similar to DR rats, but not sgk1. These observations suggest that the sgk1-mediated alpha-ENaC-inducing action of aldosterone normally observed in salt-resistant rats is disordered in salt-sensitive hypertensive rats, and that an sgk1-independent alpha-ENaC-inducing mechanism would cause hypertension in a salt-sensitive aldosterone-independent manner in DS rats. Supported by JSPS 15659052 (YM), 15590189 (NN), 15790120 (HM). [Jpn J Physiol 54 Suppl:S134 (2004)]
