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Effects of Na/K‐ATPase on cardiac remodeling and regeneration in partial nephrectomized mice

Na/K‐ATPase plays an important role in uremic cardiomyopathy. Reduction of Na/K‐ATPase attenuates survival signaling in cardiac cells. This study tested the role of Na/K‐ATPase in partial nephrectomized (PNx) Na/K‐ATPase α1 heterozygous mice (α1+/−) and their wild‐type (WT) littermates. PNx was established by ligation of one branch of the left renal artery, followed by removal of the entire decapsulated right kidney one week later. Results demonstrated that body weight was lower by the end of the experiment in α1+/− PNx animals (33.63 ± 2.4g vs 36 ± 1.1g in WT), while cardiac hypertrophy was evident in both PNx groups. In α1+/− mice, the heart/body weight ratio was 5.0 ± 0.38 for PNx, vs 3.8 ± 0.08 for sham, whereas in WT animals the ratio was 4.8 ± 0.28 vs 3.8 ± 0.11. PNx significantly increased blood pressure in both groups. Cardiac fibrosis, as indicated by Sirius Red staining, was increased significantly in both genetic groups versus respective shams. To examine regenerative capability cardiac tissues were probed for the progenitor cell marker c‐Kit. The α1+/− mice had a significantly higher number of c‐Kit positive cells in their heart tissue compared to WT mice. We conclude that PNx induces hypertrophic growth and fibrosis regardless of Na/K‐ATPase content. However, regeneration as indicated by c‐Kit expression seems more active in α1+/− mice. Supported by NIH HL‐105649