Myocardial (Na+,K+)-ATPase activity in Dahl salt-sensitive and resistant rats.

Vascular (Na+,K+)-pump activity (ouabain-sensitive 86Rb+ uptake) and myocardial (Na+,K+)-ATPase activity are reduced in animals with various forms of low renin, experimental hypertension. On the other hand, vascular (Na+,K+)-pump activity is increased in Dahl salt-sensitive relative to resistant rats (a genetic model of hypertension), regardless of salt intake or blood pressure and it is also increased in Dahl salt-sensitive rats on high salt (8% NaCl) relative to low salt (0.4% NaCl) diets. It has been suggested that this increase in vascular (Na+,K+)-pump activity may be secondary to an increase in the vascular sarcolemmal permeability to Na+ in these salt-sensitive rats. In the present study, (Na+,K+)-ATPase activity of left ventricular microsomal fractions, was increased in Dahl salt-sensitive relative to resistant rats on low salt diets; however, this difference disappeared when these salt-sensitive and resistant rats were placed on high salt diets. In contrast, myocardial (Na+,K+)-ATPase activity was decreased in Dahl salt-sensitive rats on high relative to low salt diets. Evidence that this decrease in (Na+,K+)-ATPase activity is not secondary to myocardial hypertrophy in the hypertensive salt-sensitive rats, and mechanisms by which decreased cardiovascular (Na+,K+)-pump activity, increased sarcolemmal permeability or both, might contribute to elevated blood pressure, are discussed.