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Hypertension, Vol 7, 423-429, Copyright © 1985 by American Heart Association
PU Feig, PP Mitchell and JW Boylan
Sodium transport by erythrocyte membranes was studied in hypertensive and
normotensive humans and in spontaneously hypertensive rats (SHR) and
normotensive Wistar-Kyoto rats (WKY). The rate constants of sodium efflux
were increased in both hypertensive humans and rats, and this increase was
due mostly to an increase in the ouabain-resistant component of efflux.
Both the furosemide-sensitive and furosemide- resistant components of
efflux were increased. The ouabain-sensitive efflux was also increased, as
confirmed by the ouabain-sensitive rubidium influx in rats. In rats, the
intracellular sodium content was also increased in the SHR with respect to
the WKY. The transport abnormalities of red cell membrane associated with
hypertension were similar in humans and rats. In rats, sodium depletion
failed to affect the transport abnormality, while sodium load made the
difference in transport between SHR and WKY undetectable. Cross-incubation
experiments, using plasma and erythrocytes of WKY and SHR, are more
suggestive of a flux abnormality that is intrinsic to the cell membrane
than of one that is humoral in nature.
ARTICLES
Erythrocyte membrane transport in hypertensive humans and rats. Effect of sodium depletion and excess
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