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Pendrin, encoded by Slc26a4 , modulates ENaC expression and function
Author(s) -
Kim YoungHee,
Pech Vladimir,
Spencer Kathryn B,
Beierwaltes William H,
Everett Lorraine A,
Green Eric D,
Shin Wonkyong,
Sutliff Roy L,
Wall Susan M
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.a902-a
Subject(s) - pendrin , epithelial sodium channel , aldosterone , medicine , endocrinology , kidney , chemistry , wild type , transporter , immunohistochemistry , mineralocorticoid , mutant , biology , sodium , gene , biochemistry , organic chemistry
Pendrin, encoded by Slc26a4 , mediates renal Cl − absorption across non‐A intercalated cells, through Cl − /HCO 3 − exchange, which increases blood pressure. Because aldosterone–induced hypertension occurs by increasing both Cl − (e.g. pendrin) and Na + transporter expression, we asked if Na + transporter expression is altered in kidney from aldosterone‐treated Slc26a4 null mice. Thus, wild type and Slc26a4 null mice were given a NaCl‐replete, a NaCl‐restricted, or a NaCl‐replete diet and aldosterone or aldosterone analogues. Expression of the major renal Na + transporters was examined using immunoblots and immunohistochemistry. Following each of these treatments, expression of NHE3, NKCC1/2, and NCC were similar in mutant and wild type mice. Renal ENaC subunit expression increased, as expected, in response to aldosterone in both Slc26a4 null and wild type mice. However, expression of all 3 ENaC subunits and ENaC‐mediated current were markedly reduced in kidneys from Slc26a4 null relative to wild type mice under each condition tested. ENaC expression was similar, however, in thyroid tissues from wild type and mutant mice. We conclude that within kidney, but not thyroid, pendrin modulates ENaC expression. This reduced ENaC expression likely contributes to the lower blood pressure in Slc26a4 null mice in response to aldosterone.