Pathophysiological role of cation transport and natriuretic factors in hypertension.

This review considers in some detail the hypothetical relationships between sodium fluxes, both active and passive, across the cell membrane, and intracellular sodium concentration in vascular smooth muscle in the animal models of hypertension. It appears that two basic types of transport defects, increased cell membrane permeability to sodium and decreased active pumping of sodium at a given internal sodium concentration, can exist in vascular smooth muscle in experimental hypertension, and that sometimes the two defects coexist, further increasing internal sodium concentration. It is possible that eventually we may find similar transport defects in vascular smooth muscle in humans with arterial hypertension. Decreased active pumping at a given internal sodium concentration appears to result from a humoral sodium pump inhibitor. Future directions for research in the area are also considered. First priority should be given efforts to determine the chemical structure of the sodium pump inhibitor(s). High priority should also be given to attempts to measure passive and active sodium fluxes and intracellular sodium concentration in vascular smooth muscle cells in vivo, and to determine the role of atrial natriuretic factor in the genesis and maintenance of hypertension.