Abstract
Abstract
Ouabain-sensitive 86rubidium uptake was used to estimate sodium-potassium pump activity in the tail arteries of Dahl salt-sensitive and Dahl salt-resistant rats on normal and high oral intakes of salt. Uptake was increased in the salt-sensitive strain relative to the resistant strain at a given salt intake. It was also increased in a given strain when the salt intake was increased. In each case the increased ouabain-sensitive uptake was associated with increased ouabain-insensitive uptake which in part reflects the permeability of the cell membrane to rubidium. The results suggest that the increased pump activity is a secondary compensatory response to increased passive penetration of sodium. In this respect, the Dahl salt-sensitive rat is similar to SHR, another genetic model, but different from the other low-renin, presumably, volume-expanded models of hypertension we have studied.
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