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.
Highlights
According to the 2016 American Heart Association (AHA) Statistical Update [1], 32.6% of people in the United States aged 20 and older have hypertension, and about 54.1%of those cases have their hypertension well-controlled
Based on the observations of the interplay amongst cardiotonic steroids (CTS), reactive oxygen species (ROS) and Na/K-ATPase signaling, we have proposed that Na/K-ATPase, along with its ion-pumping and signaling function, functions as an amplifier/receptor for oxidant signals, by coupling with c-Src (Figure 1)
While Na/K-ATPase is the specific target of CTS, oxidative stress and CTS-induced increases in ROS can target systems other than the Na/K-ATPase/c-Src complex
Summary
According to the 2016 American Heart Association (AHA) Statistical Update [1], 32.6% 2008 AHA Scientific Statement [2], excessive dietary salt ingestion contributes to the development and maintenance of hypertension and tends to be more pronounced in older salt-sensitive people, African. Americans, and those with chronic kidney diseases [3,4,5]. In the 2016 AHA Scientific Statement [6], salt sensitivity was defined as a physiological trait by which blood pressure (BP) changes are parallel to changes in salt intake. United States Department of Agriculture (USDA) Guidelines and AHA Scientific Statements all suggest that a modest dietary salt reduction along with a balanced diet would be beneficial in BP control.
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