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Pioglitazone‐induced sodium retention in rat is independent of alpha subunit of epithelial sodium channel (ENaCá) expression in distal nephron
Author(s) -
Ma Hongbao,
Ponnam Bala,
Li Jinping,
Chou ShyanYih
Publication year - 2011
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.25.1_supplement.1041.30
Subject(s) - endocrinology , epithelial sodium channel , medicine , chemistry , pioglitazone , aldosterone , sodium , thiazolidinedione , renal cortex , nephron , kidney , biology , organic chemistry , type 2 diabetes , diabetes mellitus
We studied the role of ENaC‐alpha in renal sodium retention induced by pioglitazone (PGZ), a thiazolidinedione hypoglycemic agent. Male Sprague‐Dawley rats in metabolic balance cages were fed on a 1% NaCl diet (control group) and the experimental group received the same diet plus PGZ (40 mg/kg bw/day for 5 days). To suppress aldosterone production, rats were fed on a 3% NaCl diet with or without PGZ. To further suppress aldosterone production, enalapril (25 mg/kg bw/day) was added to olmesartan (15 mg/kg bw/day). Western blotting of the membrane‐enriched fractions from the renal cortex and medulla was performed and ENaCα density normalized to beta‐actin measured. PGZ treatment led to sodium retention. In 4 control rats on a 1% NaCl diet, ENaCα expression was 0.54±0.02 in the medulla, similar to 0.60±0.04 in 4 PGZ‐treated rats, and was 0.68±0.11 in the cortex in PGZ‐treated rats, similar to 0.75±0.16 in the control rats. In the rats fed on a 3% NaCl diet, the ENaCα expression was similar in PGZ‐treated and control rats both in the medulla and cortex. In PGZ‐treated rats receiving a 3% NaCl diet, enalapril and olmesartan, ENaCα expression in the medulla and cortex was also similar in PGZ‐treated and control rats. These results show that sodium retention induced by PGZ is independent of ENaCα expression in the apical membrane of the distal nephron, a finding also extended to the situations where aldosterone production is suppressed. Research support: institutional research fund