Abstract
Disturbance of renal Na+ reabsorption develops hypertension in Dahl salt-sensitive (DS) rat. Aldosterone plays a critical role in controlling renal Na+ reabsorption by stimulating expression of epithelial Na+ channel (ENaC) and also activate an ENaC-regulating protein kinase, serum and glucocorticoid-regulated kinase 1 (SGK1). Therefore, we studied how aldosterone regulates ENaC expression and SGK1 in DS rat. Aldosterone (1.5 mg/kg B.W.) was subcutaneously injected into adrenalectomized DS and Dahl salt-resistant (DR) rats kept with normal (0.3% NaCl) diet and saline for 2 weeks after adrenalectomy. RNA and protein were extracted from the kidney 6 hr after the aldosterone application. Aldosterone decreased mRNA expression of β- and γ-ENaC in DS rat unlike DR rat, while aldosterone increased α-ENaC mRNA expression in DS rat similar to DR rat. Further, we found that aldosterone did not affect SGK1 expression in DS rat but elevated it in DR rat. These observations indicate that ENaC and SGK1 are abnormally regulated by aldosterone in DS rats, suggesting that these abnormal responses to aldosterone would be one of factors causing salt-sensitive hypertension. Supported by JSPS 17390057, 17590191, 17790154. [J Physiol Sci. 2006;56 Suppl:S160]
