Reduced Sodium Pump alpha1, alpha3, and beta1-Isoform Protein Levels and Na+, K+-ATPase Activity but Unchanged Na+-Ca2+ Exchanger Protein Levels in Human Heart Failure

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Abstract

Background

Cardiac glycosides initiate an increase in force of contraction by inhibiting the sarcolemmal sodium pump (Na+,K+-ATPase), thereby decreasing Ca2+ extrusion by the Na+-Ca2+ exchanger, which increases the cellular content of Ca2+. In patients with heart failure the sensitivity toward cardiac glycosides is enhanced.

Conclusions

The enhanced sensitivity of failing human myocardium toward cardiac glycosides may be, at least in part, attributed to a reduced protein expression and activity of the sarcolemmal Na+,K+-ATPase without a change in Na+-Ca (2+) exchanger protein expression. (Circulation. 1999;99:2105-2112.)

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