Contribution of renal epithelial sodium channel in sodium retention during chronic heart failure

TL;DRAbstract

The goal of the present study was to examine the contribution of renal epithelial sodium channel (ENaC) in the increased sodium and water retention during chronic heart failure (CHF). We hypothesized that over expression of ENaC could be involved in sodium retention during CHF. The left coronary ligation‐induced heart failure model in the rat was used. There was significant increase in diuretic (7‐fold of sham) and natriuretic responses (3‐fold of sham) to the ENaC inhibitor benzamil in the rats with CHF compared to sham rats. Real‐time PCR and Western blotting demonstrated that the mRNA and protein abundance of α, β, and γ‐subunits of ENaC were significantly increased in the cortex (α‐ENaC: mRNA Δ104±24%, protein Δ32±7% compared to sham rats) and outer medulla (α‐ENaC: mRNA Δ52±18%, protein Δ33±9% compared to sham rats) in CHF compared to sham rats. Immunohistochemical imaging confirmed the increased labeling of α‐ENaC, β‐ENaC and γ‐ENaC subunits in the collecting duct segments in rat

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