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High salt diet stimulates ENaC in Dahl salt‐sensitive rats
Author(s) -
Bao HuiFang,
Yue Qiang,
Eaton Douglas,
Zhang ZhiRen,
Ma HePing
Publication year - 2013
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.27.1_supplement.913.42
Subject(s) - epithelial sodium channel , medicine , endocrinology , nephron , reactive oxygen species , oxidative stress , downregulation and upregulation , chemistry , sodium , kidney , biology , biochemistry , gene , organic chemistry
It has long been suggested that the renal epithelial sodium channel (ENaC) contributes to the development of salt‐sensitive hypertension. However, it remains unclear whether high salt diet can stimulate ENaC in Dahl salt‐sensitive (DS) rats (a model of salt‐sensitive hypertension). Our confocal microscopy data showed that high salt diet decreased ENaC expression in the cortical collecting ducts (CCD) of control rats, but increased ENaC expression in the CCD of DS rats. Interestingly, high salt diet also altered ENaC plasticity along the renal tubules by inducing ENaC expression in the thick ascending limb of DS rats, but not of control rats. Our cell‐attached patch‐clamp data showed that high salt diet increased ENaC open probability in the split‐open CCD of DS rats, but not of control rats. Since it is known that high salt diet elevates reactive oxygen species (ROS) in the kidneys of DS rats and our recent studies have shown that hydrogen peroxide (one form of ROS) stimulates ENaC in cultured distal nephron cells, high salt diet may stimulate ENaC in CCD and induce ENaC expression in the thick ascending limb by causing oxidative stress in the kidneys of DS rats (supported by NIH 5R01‐DK067110 to HPM).