Na(+), K(+)-ATPase (NKA) is well known for its function as an ion pump. Studies during the last decade have revealed an additional role for NKA as a signal transducer. In this brief review, we describe how cardiotonic steroids, which are highly specific NKA ligands, trigger slow Ca(2+) oscillations by promoting the interaction between NKA and the inositol trisphosphate receptor, and how this Ca(2+) signal activates the NF-κB subunit p65 and increases the expression of the antiapoptotic factor Bcl-xL. The potential tissue-protective effects of this signal are discussed.
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