Reciprocal regulation of cardiac Na-K-ATPase and Na/Ca exchanger: hypertension, thyroid hormone, development

Inhibiting cardiac Na pump activity decreases the driving force for the Na/Ca exchanger transport that increases cellular Ca stores and contractility. Decreased abundance of Na pumps would be expected to have the same effect as decreased activity unless there was reciprocal regulation of Na/Ca exchanger expression to oppose the effects of depressed Na pump activity on intracellular Ca stores. The aim of this study was to test the hypothesis that cardiac Na/Ca exchanger abundance is regulated in a reciprocal fashion to Na-K-ATPase abundance in a number of models known to have altered Na-K-ATPase abundance. In renovascular hypertension, cardiac ventricular Na-K-ATPase alpha 1-levels are unaltered, alpha 2-isoform subunit mRNA and protein levels decrease to 0.76 +/- 0.06 and 0.56 +/- 0.07 of control, respectively, and the Na/Ca exchanger protein (not mRNA) increased 1.35 +/- 0.11-fold. In the transition from hypothyroid to hyperthyroid cardiac alpha 1 doubles, alpha 2-protein increases 8.83 +/- 1.06-fold, an...