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Expression Of Epithelial Sodium Channel (ENaC) And Its Regulatory Genes In Brain Of Dahl S And R Rats On High Salt Diet.
Author(s) -
Reza Erona,
Wang HongWei,
Leenen Frans H H
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1407-d
Subject(s) - epithelial sodium channel , sgk1 , medicine , endocrinology , aldosterone , messenger rna , gene expression , sodium , chemistry , biology , gene , glucocorticoid , biochemistry , organic chemistry
Central blockade of ENaC or MR prevents sympathoexcitation and hypertension in Dahl S rats on high salt diet. We assessed the effects of high salt on expression of ENaC and its regulators ie‐ MR, SGK1, as well as aldosterone synthase (AS) and 11 β HSD2 mRNA in brain areas of S and R rats. 4 weeks old Dahl S and R rats were placed on regular (0.3%) or high (8%) salt diet for 2 and 4 weeks. mRNA expression was measured by real time RT‐PCR. In the choroid plexus (CP) and PVN, ENaC subunits transcription was not affected by salt intake. 2 weeks high salt diet increased SGK1 mRNA in CP of both strains and in PVN of only S rats. In the SON, high salt significantly increased β ENaC and SGK1 mRNA in S rats at 2 weeks and tended to increase at 4 weeks. Expression of γ ENaC and 11 βHSD2 in SON were increased by high salt in both strains at 2 weeks, persisted to be increased only in S rats at 4 weeks. Salt intake did not affect MR and AS expression. High salt induced increase in SGK1 and ENaC expression in brain areas such as SON of S rats may increase ENaC activity and thereby enhance neuronal excitability leading to sympathoexcitation and hypertension.