Abnormal erythrocyte cation transport in primary hypertension. Clinical and experimental studies.

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Abstract
Several abnormalities concerning sodium (Na+) transport in erythrocytes of essential hypertensive patients have been recently observed. An abnormal extrusion of an erythrocyte Na+ load was described in our laboratory. This defect appeared to be specific for essential hypertension since it was absent in the secondary forms of the disease. The present investigation was performed on 194 Caucasian subjects with essential hypertension or born of hypertensive parents, 86 normotensive controls, and 14 families (78 subjects) studied over two to three generations. The distribution pattern of the erythrocyte defect is compatible with the expression of a single gene transmitted according to an autosomic and dominant mode. To confirm the genetic association between the red blood cell abnormality and primary hypertension, genetically hypertensive rats were investigated in parallel to our clinical studies. A reduction in the net Na+ extrusion from red blood cells was found in two varieties of genetic hypertension (SHR and H-prone-Na+-sensitive Sabra rats). The abnormality could be detected before the development of a significant hypertension. When these various rat sub-strains were acutely or chronically loaded with Na+ (either intraperitoneally or orally), a significant increase in erythrocyte Na+ content was observed only in those substrains having a genetic propensity to develop hypertension. This finding, which appears to be a consequence of the reduction in net Na+ efflux, is of interest for several reasons. It confirms the existence of a close association between a genetic predisposition to develop high blood pressure and cell Na+ retention in the presence of an excess Na+ intake. It draws attention to the possible role of intracellular Na+ in the pathogenesis of primary hypertension. Of more practical importance, the abnormal Na+ handling in erythrocytes may be a genetic marker of primary hypertension.