Red cell ouabain-resistant Na+ and K+ transport in Wistar, Brown Norway and spontaneously hypertensive rats.

Our previous studies concerning the role of furosemide-resistant cation leaks in genetic hypertension demonstrated that blood pressure of recombinant inbred strains (derived from F2 hybrids of spontaneously hypertensive and normotensive Brown Norway rats) cosegregated with inward Na+ leak (determined in saline medium) but not with Na+ efflux (measured in Mg(2+)-sucrose medium) or with Rb+ uptake (found in either medium). In the present study the alterations of particular components of ouabain-resistant (OR) Na+ and K+ (Rb+) transport in erythrocytes of spontaneously hypertensive rats (SHR) were analyzed using saline and Na(+)-free (Mg(2+)-sucrose or choline) incubation media. OR Na+ net uptake was elevated in SHR as compared to both normotensive strains--Brown Norway and Wistar rats. This was mainly due to an increased bumetanide-resistant (BR) Na+ inward leak. On the other hand, Wistar rats did not differ significantly from SHR in either OR Na+ efflux or OR Rb+ uptakes. Major augmentations of BR Na+ efflux and BR Rb+ uptake in SHR erythrocytes were seen not only in Mg(2+)-sucrose medium but also in choline medium. In both Na(+)-free media there was a considerable saturable Na+i-dependent component of BR Na+ and Rb+ fluxes which was more pronounced in SHR than in BN erythrocytes. A great caution is required for the interpretation of the data on "increased passive membrane permeability" obtained in SHR erythrocytes incubated in Na(+)-free media because of the presence of this saturable component which seems to be related to incompletely inhibited Na(+)-K+ pump.(ABSTRACT TRUNCATED AT 250 WORDS)