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Responses of blood pressure to alterations in the intake of sodium chloride vary widely between individuals. This variable responsiveness complicates investigations of mechanisms responsible for salt sensitivity and limits the appeal of salt restriction as a nonpharmacological antihypertensive therapy. There is therefore considerable interest in the development of markers of salt sensitivity, and several general anthropometric, racial, and biochemical features of salt-sensitive groups have been described. As yet, however, no single test or combination of features permits reliable prediction in individual patients of the responsiveness of blood pressure to chronic salt loading or depletion. During the 1980s, burgeoning interest in the role of cellular Na content and transmembrane Na fluxes in essential hypertension led to the numerous studies reviewed below that attempted to define the relation of blood pressure responsiveness to shortand longterm changes in salt balance to membrane markers. Investigations of a possible role for membrane transport in the control of blood pressure responses to salt loading and depletion have addressed two major issues. The majority of studies have examined the question of whether acute or chronic changes in salt balance cause changes in cellular Na content or transport. Less well studied is the issue of whether baseline cellular cation handling characteristics are predictive of future blood pressure responses to dietary salt modification. The few studies that have examined this latter point are of particular interest in light of the growing appreciation that some heterogeneities in cellular cation metabolism apparently reflect genetic lesions that may prove to predispose to hypertension. In other words, there may be genetically determined cellular phenotypes that predict salt sensitivity of blood pressure.

Membrane sodium transport and salt sensitivity of blood pressure.