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  • Title: Erythrocyte membrane sodium transport in patients with treated and untreated essential hypertension.
    Author: Cole CH.
    Journal: Circulation; 1983 Jul; 68(1):17-22. PubMed ID: 6303625.
    Abstract:
    Various parameters of erythrocyte membrane sodium transport were measured in patients with untreated essential hypertension, in the normotensive offspring of parents with hypertension, and in patients whose hypertension had been controlled by medication. Net sodium efflux, measured by an isotopic tracer technique, was 2.12 +/- 0.17 mM Na+/1 of red blood cells (RBCs)/hr in patients with untreated essential hypertension, compared with 1.55 +/- 0.12 mM Na/1 of RBCs/hr in a group of normotensive controls (p less than .025). Partitioning sodium efflux into ouabain-sensitive and ouabain-insensitive components revealed a significant elevation of both components of membrane sodium transport in the patients with untreated essential hypertension. Ouabain-sensitive sodium efflux was 1.38 +/- 0.09 mM Na/1 RBCs/hr in the patients, compared with 1.04 +/- 0.07 mM Na/1 RBCs/hr in the controls. Ouabain-insensitive sodium efflux was also increased from 0.51 +/- 0.05 mM Na/1 RBCs/hr in the controls to 0.74 +/- 0.09 mM Na/1 RBCs/hr in those with untreated hypertension. Despite these changes in sodium efflux, Na,K-ATPase activity in the erythrocyte membrane, measured at maximum velocity (Vmax), was normal, suggesting that the observed abnormalities in membrane sodium transport in patients with untreated essential hypertension resulted from a change in pump control mechanisms rather than a change in enzyme activity. With the techniques used in this study we were unable to identify changes in erythrocyte membrane transport in the normotensive offspring of hypertensive parents. Membrane sodium transport was also examined in hypertensive patients whose blood pressure had been controlled by medication. In this group it was found that erythrocyte sodium transport did not differ from that in our control group, which suggests that treatment of hypertension can modify fundamental pathophysiologic changes at the level of the cell membrane.
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