RED-CELL OUABAIN-RESISTANT NA-NORWAY AND SPONTANEOUSLY HYPERTENSIVE RATS( AND K+ TRANSPORT IN WISTAR, BROWN)

Our previous studies concerning the role of furosemide-resistant catio n leaks in genetic hypertension demonstrated that blood pressure of re combinant inbred strains (derived from F2 hybrids of spontaneously hyp ertensive and normotensive Brown Norway rats) cosegregated with inward Na+ leak (determined in saline medium) but not with Na+ efflux (measu red in Mg2+-sucrose medium) or with Rb+ uptake (found in either medium ). In the present study the alterations of particular components of ou abain-resistant (OR) Na+ and K+ (Rb+) transport in erythrocytes of spo ntaneously hypertensive rats (SHR) were analyzed using saline and Na+- free (Mg2+-sucrose or choline) Incubation media. OR Na+ net uptake was elevated in SHR as compared to both normotensive strains - Brown Norw ay and Wistar rats. This was mainly due to an increased bumetanide-res istant (BR) Na+ inward leak. On the other hand, Wistar rats did not di ffer significantly from SHR in either OR Na+ efflux or OR Rb+ uptakes. Major augmentations of BR Na+ efflux and BR Rb+ uptake in SHR erythro cytes were seen not only in Mg2+-sucrose medium but also in choline me dium. In both Na+-free media there was a considerable saturable Na+i-d ependent component of BR Na+ and Rb+ fluxes which was more pronounced in SHR than in BN erythrocytes. A great caution is required for the in terpretation 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. It can be concluded on the basis o f BR fluxes seen in erythrocytes incubated in saline media which proba bly reflect true cation leaks that passive membrane permeability of SH R erythrocytes is increased for Na+ but not for Rb+(K+).