Na/K-ATPase Signaling and Salt Sensitivity: The Role of Oxidative Stress

Abstract

Other than genetic regulation of salt sensitivity of blood pressure, many factors have been shown to regulate renal sodium handling which contributes to long-term blood pressure regulation and have been extensively reviewed. Here we present our progress on the Na/K-ATPase signaling mediated sodium reabsorption in renal proximal tubules, from cardiotonic steroids-mediated to reactive oxygen species (ROS)-mediated Na/K-ATPase signaling that contributes to experimental salt sensitivity.

Keywords: Na/K-ATPase; ROS; cardiotonic steroids; renal sodium handling; salt sensitivity; signaling.

Figure 1

Illustration of the Na/K-ATPase signaling-mediated oxidant amplification loop, showing increases in cardiotonic steroids (CTS) (A) or increases in ROS within physiological range (B); stimulated oxidant amplification loop. Increases in CTS alone or increases in ROS alone or a combination of increases in CTS and ROS (not shown) stimulate Na/K-ATPase/c-Src signaling to induce Na/K-ATPase signaling-mediated events, such as renal sodium handling in proximal tubules (natriuresis), PNx-induced uremic cardiomyopathy and a high fat diet-induced adipogenesis.