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Sodium transport in hypertension.

Although most workers in the field agree that salt causes hypertension, but there is no well-established mechanism(s) explaining how salt works. Vast literature exists on abnormal sodium (Na+) transport processes in human and experimental hypertension from various cell systems. We examined the recent developments in the investigation of three important sodium transport pathways: Na+/K+ pump, Na+/Li+ countertransport and Na+/K+ cotransport in hypertension. The activities of these transporters may affect vascular reactivity or may serve as genetic marker for essential hypertension. Selected reports on the abnormalities of these transporters were summarized, potential problems in the interpretation of these data were discussed, and the current view about the physiological or pathophysiological meaning of these studies were presented. The multiple sites of defects and sometime conflicting reports on Na+ transport in hypertension also lead to alternative hypothesis associating membrane abnormalities with hypertension. Two models, considering membrane lipid bilayers and cellular calcium handling as primary sites of defect and the related evidence, were introduced. Finally, the role of natriuretic hormone (or endogenous Na+ pump inhibitor) in influencing Na+ transport was briefly discussed.