Alterations in active Na-K transport during mineralocorticoid-salt hypertension in the rat.

Studies have been conducted to determine which, if any, of the parameters governing active Na-K transport (K and/or ouabain sensitive) are altered in vascular smooth muscle during mineralocorticoid-salt hypertension. Rats with one kidney removed were treated with either aldosterone or deoxycorticosterone acetate plus saline for 3-4 wk. Ion transport was measured in arteries incubated in a physiological salt solution for periods of 4-6 h. Increased active Na efflux was observed in femoral arteries and aortas from the hypertensive group. This alteration resulted primarily from an elevation in the saturation or maximal capacity of the active transport mechanism, which operated with no significant change in cell Na concentration. The transport parameters related to ion selectivity, cooperativity, and temperature dependence were not significantly altered. Measures of active Na efflux and K influx in the same aortic strips indicated that both fluxes were elevated in the hypertensive group. The ratio of Na to K for active transport was significantly greater than one but was unchanged in the hypertensive rats. These studies provide evidence for the electrogenic operation of the Na-K pump in arterial smooth muscle and for the operation of the pump at a higher level during mineralocorticoid-salt hypertension. This alteration may result from increased turnover of individual sites or possibly the incorporation of more sites into the membrane as a result of mineralocorticoid-salt treatment.