Cardiotonic steroids play a key role in sodium excretion in response to volume expansion. Their effect is mediated through their binding to the Na/K-ATPase, a membrane ion transporter which has recently been found to serve as scaffolding and signaling protein. These scaffolding and signaling functions not only stimulate natriuresis through the endocytosis of key ion transporters, namely the sodium proton antiporter isoform 3 (NHE3) and itself, but also produces pro-fibrotic effects. The focus of this editorial is to the tradeoff this creates between natriuresis in the short term and progression of cardiac and renal fibrosis in the long term.
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Last date updated on September, 2014
