Abnormal expression of ENaC and SGK1 mRNA induced by dietary sodium in Dahl salt‐sensitively hypertensive rats
Authors:
- Naomi NiisatoNNNaomi Niisato
- Yukinori SawabeYSYukinori Sawabe
- Hiroaki MiyazakiHMHiroaki Miyazaki
- Shinsaku TokudaSTShinsaku Tokuda
- Kyosuke NishioKNKyosuke Nishio
- Toshikazu YoshikawaTYToshikazu Yoshikawa
- Yoshinori MarunakaYoshinori Marunaka
- 1 October 2007
- journal article
- Published by Wiley in Cell Biology International
- Vol. 31 (10) , 1288-1291
Abstract
Epithelial sodium channel (ENaC) plays a crucial role in controlling sodium reabsorption in the kidney keeping the normal blood pressure. We previously reported that the expression of ENaC mRNA in the kidney of Dahl salt‐sensitive (DS) rats was abnormally regulated by aldosterone, however it is unknown if dietary sodium affects the expression of ENaC and serum and glucocorticoid‐regulated kinase 1 (SGK1), which plays an important role in ENaC activation, in DS rats. In the present study, we investigated whether dietary sodium abnormally affects the expression of ENaC and SGK1 mRNA in DS rats. DS and Dahl salt‐resistant (DR) rats (8 weeks old) were divided into three different groups, respectively: (1) low sodium diet (0.005% NaCl), (2) normal sodium diet (0.3% NaCl), and (3) high sodium diet (8% NaCl). The high sodium diet for 4 weeks in DS rats elevated the systolic blood pressure, but did not in any other groups. The expression of α‐ENaC mRNA in DS rats was abnormally increased by high sodium diet in contrast to DR rats, while it was normally increased by low sodium diet in DS rats similar to DR rats. The expression of β‐ and γ‐ENaC mRNA in DS rats was also abnormally increased by high sodium diet unlike DR rats. The expression of SGK1 mRNA was elevated by high sodium diet in DS rats, but it was decreased in DR rats. These observations indicate that the expression of ENaC and SGK1 mRNA is abnormally regulated by dietary sodium in salt‐sensitively hypertensive rats, and that this abnormal expression would be one of the factors causing salt‐sensitive hypertension.Keywords
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