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Adaptive Changes of Sodium and Potassium Transporters in CRF Rat Kidneys
Author(s) -
Kim Sejoong,
Heo Nam Ju,
Jeong Ji Yong,
Oh Yun Kyu,
Na Ki Young,
Joo Kwon Wook,
Han Jin Suk
Publication year - 2008
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.22.1_supplement.934.12
Subject(s) - medicine , endocrinology , excretion , sodium , chemistry , potassium , epithelial sodium channel , kidney , urinary system , urea , transporter , biochemistry , organic chemistry , gene
In chronic renal failure (CRF), residual nephrons can magnify their excretion of sodium and potassium. However, long‐term adaptive mechanism of renal tubular transporters in CRF has not been fully evaluated. We performed immunoblotting and immunocytochemistry, thus investigating the sequential changes of expression of major renal sodium and potassium transporters in rats from 4 weeks to 12 weeks after 5/6 nephrectomy (Nx). At 4 weeks, the density of NKCC2, NCC, ENaC‐α, and ENaC‐γ in CRF rats significantly increased (477%, 222%, 451%, and 435% of control, respectively) although the expression of NHE3 and SGLT1 did not altered. In contrast, expression of NKCC2 and NCC markedly decreased at 12 weeks (55.4% and 30.8%, respectively), and NHE3 and SGLT1 also decreased at 12 weeks (48.4% and 24.6%, respectively). The protein abundance of ENaC‐α significantly increased during the whole period. Urinary potassium excretion rate was well‐correlated with urinary urea or sodium excretion rate, although immunoblotting of ROMK and Na‐K‐ATPase showed a gradual decrease in the late stages of CRF. We suggest that this sequential decrease of major renal sodium transporters may be a main mechanism for increased urinary sodium excretion, and that increased urea excretion rates or distal sodium delivery may be a major explanation for increased urinary potassium excretion in CRF rats.