Relation of Cell Permeability to Salt Sensitivity in Hypertension

Abstract

More than 30 years ago we proposed that mineralocorticoid hypertension begins with increased permeability of the vascular smooth muscle cell, followed by the progressive accumulation of sodium, and the restructuring of the cell to cope with the load [1]. Although supportive evidence from many laboratories continued to accumulate over the years, direct evidence for increased sodium permeability and transport as primary events in the hypertensive response to deoxycorticosterone acetate (DOCA) was obtained only 3 years ago [2]. This was followed in the next year by the demonstration that over the first 16 days of treatment with this mineralocorticoid, blood pressure was directly related to cell [Na] and inversely related to the transmembrane Na gradient, as had earlier been predicted [3].

This work was carried out with the aid of a grant from the Medical Research Council of Canada.