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AJP - Heart and Circulatory Physiology, Vol 252, Issue 1 1-H6, Copyright © 1987 by American Physiological Society
ARTICLES |
J. Diez, P. Hannaert and R. P. Garay
The interaction of the Na+-K+ pump with internal Na+ was investigated in erythrocytes from 38 normotensive control subjects and 49 essential hypertensive patients. In six of the hypertensive patients, the Na+-K+ pump exhibited an apparent dissociation constant for internal Na+ (KNa) above an upper normal limit of 7 mmol/l cells. Four of these six hypertensives showed an increase in the maximal rate of ouabain-sensitive Na+ efflux (Vmax), above an upper normal limit of 11 mmol X l cells-1 X h-1. These abnormalities were stable in repeated determinations over 1-3 yr. A kinetic study of other erythrocyte Na+ transport pathways showed that 16 hypertensives had a low apparent affinity of the Na+-K+ cotransport system for internal Na+, 10 hypertensives exhibited increased Na+-Li+ countertransport fluxes, and 11 hypertensives had increased Na+ leak. None of these three abnormalities were observed in the six hypertensives with abnormal pump fluxes. We thus propose to denominate them as Pump (-) hypertensives. Interestingly, four Pump (-) hypertensives exhibited an increased maximal rate of outward Na+-K+ cotransport. Basal erythrocyte Na+ content of Pump (-) hypertensives was within normal range. This suggests that the increased maximal rates of the Na+-K+ pump and Na+-K+ cotransport system compensate the low pump affinity for internal Na+.
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