高钠浓度和钒酸盐对大鼠心脏和肾脏钠钾ATP酶的抑制作用。

Inhibition of rat cardiac and renal Na+,K+-ATPase by high sodium concentrations and vanadate.

作者信息

Clough D L

出版信息

Life Sci. 1985 Sep 2;37(9):799-807. doi: 10.1016/0024-3205(85)90514-4.

Abstract

In the present study, rat renal Na+,K+-ATPase was found to be more sensitive to inhibition by high Na+ concentrations (100-400 mM) than was rat cardiac Na+,K+-ATPase. K+ was more effective in reversing the inhibition by Na+, of cardiac relative to renal Na+,K+-ATPase. Rat renal Na+,K+-ATPase was also more sensitive than cardiac Na+,K+-ATPase to inhibition by vanadate over this range of Na+ concentrations. These results support the hypothesis that vanadate may selectively regulate Na+,K+-ATPase in the kidney, and they may also help explain the natriuretic and diuretic effects of vanadate in rats. Inhibition of renal Na+,K+ATPase by Na+, may also help explain, in part, the natriuretic and diuretic effects of acute saline loading.

摘要

在本研究中，发现大鼠肾Na⁺,K⁺-ATP酶比大鼠心脏Na⁺,K⁺-ATP酶对高浓度Na⁺（100 - 400 mM）的抑制作用更敏感。相对于肾Na⁺,K⁺-ATP酶，K⁺在逆转心脏Na⁺,K⁺-ATP酶受Na⁺抑制方面更有效。在该Na⁺浓度范围内，大鼠肾Na⁺,K⁺-ATP酶也比心脏Na⁺,K⁺-ATP酶对钒酸盐的抑制作用更敏感。这些结果支持钒酸盐可能选择性调节肾脏中Na⁺,K⁺-ATP酶的假说，并且它们也可能有助于解释钒酸盐对大鼠的利钠和利尿作用。Na⁺对肾Na⁺,K⁺-ATP酶的抑制作用也可能部分有助于解释急性盐水负荷的利钠和利尿作用。