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Enhanced expression of renal AQP2 and ENaC in rats with chronic heart failure: a role for renal nerves
Author(s) -
Zheng Hong,
Fleecs Jacob,
Liu Xuefei,
Patel Kaushik P
Publication year - 2016
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.30.1_supplement.1005.4
Subject(s) - epithelial sodium channel , aquaporin 2 , medicine , sodium–hydrogen antiporter , endocrinology , kidney , western blot , denervation , sodium , ligation , heart failure , chemistry , water channel , biochemistry , mechanical engineering , organic chemistry , engineering , inlet , gene
Previously we have shown that increased expression of renal epithelial sodium channels (ENaC) subunits may contribute to the renal sodium and water retention observed during chronic heart failure (CHF). The goal of this study was to examine whether renal denervation (RDN) changes the expression of aquaporin 2 (AQP2) and two major renal sodium transporters ENaC and sodium‐hydrogen exchanger‐3 proteins (NHE3)] in rats with CHF. CHF was produced by left coronary artery ligation in rats. Four weeks after ligation surgery, bilateral RDN were performed. Western blot analysis indicated that RDN (one week later) significantly reduced enhanced protein levels of AQP2 (1.30±0.20 vs. 0.33±0.09, P<0.05), alpha‐ENaC (0.43±0.09 vs. 0.25±0.06, P<0.05), beta‐ENaC (0.11±0.03 vs. 0.05 ± 0.01, P<0.05) and gamma‐ENaC (0.89±0.15 vs. 0.44±0.09, P<0.05) subunits in the renal cortex of CHF rats compared to the CHF non‐denervated group. RDN had no significant effects on the protein expression of kidney NHE3 in both sham and CHF rats. These findings suggest a critical role for renal nerves in the enhanced expression of AQP2 and ENaC and subsequent pathophysiology of renal water and sodium retention associated with CHF. Support or Funding Information Supported by NIH grants HL124104 and HL62222