Erythrocyte membrane transport in hypertensive humans and rats. Effect of sodium depletion and excess.

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.