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 Na4 leak (determined in saline medium) but not with Na4" efflux (measured in Mg2+-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 K4 (Rb+) transport in erythrocytes of spontaneously hypertensive rats (SHR) were analyzed using saline and Na + -free (Mg24-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) Na4 inward leak. On the other hand, Wistar rats did not differ significantly from SHR in either OR Na4 efflux or OR Rb4 uptakes. Major augmentations of BR Na4 efflux and BR Rb4 uptake in SHR erythrocytes were seen not only in Mg24-sucrose medium but also in choline medium. In both Na4-free media there was a considerable saturable Na4¡-dependent component of BR Na4 and Rb4 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 Na4-free media because of the presence of this saturable component which seems to be related to incompletely inhibited Na4-K4 pump. It can be concluded on the basis of BR fluxes seen in erythrocytes incubated in saline media which probably reflect true cation leaks that passive membrane permeability of SHR erythrocytes is increased for Na4 but not for Rb4(K+).