Sodium-Potassium ATPase in Deoxycorticosterone-Salt Hypertension: Opposing Effects of Sodium Load and Mineralocorticoids

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Abstract
Previous studies of the Na-K pump in the deoxycorticosterone (DOC)-salt (DS) model of hypertension yielded contrasting results, some investigators reporting increased and others finding decreased pump activity. To test the possibility that the net pump activity in the DS rats results from separate effects of Na overload and mineralocorticoid activity, the Na+-K+-ATPase pump in DS rats was compared with that in other experimental models in which these potential determinants do not coincide. Renocortical and myocardial ATPase activities were measured in control rats; adrenalectomized-saline-repleted rats; adrenalectomized aldosterone- or dexamethasone-repleted rats; uninephrectomized, saline-drinking rats; and uninephrectomized, saline-drinking, DOC- and salt-treated rats. DOC- and salt-treated rats had higher (P < 0.001) blood pressures and lower (P < 0.05) serum K levels than control rats. Renocortical and myocardial. ATPase activities were considerably (P < 0.01) decreased in adrenalectomized, saline-repleted rats, but could be at least partially restituted by either aldosterone or dexamethasone therapy. Uninephrectomized, saline-drinking rats had reduced (P < 0.01) renocortical and myocardial ATPase activities compared with control rats. In uninephrectomized, saline-drinking rats treated with DOC, renocortical and myocardial ATPase activities were not different from control values. Apparently the Na+-K+-ATPase pump in DOC- and salt-treated rats is modulated by the opposing effects of Na overload-associated suppression and DOC-mediated stimulation.