Effects of a chronic high salt intake on blood pressure and the kinetics of sodium and potassium transport in erythrocytes of young and adult subtotally nephrectomized Sprague—Dawley rats

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Erythrocyte Na+ and K+ transport mediated by the Na+–K+ pump, the Na +,K + cotransport system and cation leaks, together with blood pressure, were determined in young and adult rats subjected to either chronic salt deprivation or chronic salt loading combined with subtotal nephrectomy. The kinetics of ion transport were studied in Na+ media as a function of extracellular K +, replaced by extracellular Rb +, and intracellular Na+ varied around the physiological range. A high salt intake increased blood pressure in young but not in adult subtotally nephrectomized rats. Erythrocyte Na+ or K+ contents of salt-deprived and salt-loaded rats did not differ. There were no major changes in Na +,K+ cotransport or cation leaks in salt-loaded rats. Chronic salt loading caused some alterations in the kinetics of the Na+–K+ pump, which were greater in young than in adult rats. The most pronounced change was a decreased affinity of the Na+–K+ pump for intracellular Na +, which was partially balanced by an increased maximal velocity. At physiological (in vivo) ion concentrations these kinetic alterations caused a slight reduction in total ouabain-sensitive Rb+ uptake [partly due to a decrease in intracellular K+:extracellular Rb+ (1:1) exchange] but no changes in Na+ net extrusion in salt-loaded rats. The erythrocyte Na+ and K + transport systems showed no changes in intrinsic properties that would favour the development or maintenance of salt hypertension in young over adult rats if similar alterations occurred in tissues relevant for blood pressure control

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