Na+ and K+ intracellular content was studied in five children with Bartter syndrome and their age and race-paired controls. Na+ and K+ pump (ouabain sensitive) fluxes, Na+-K+ co-transport (furosemide sensitive), and rate constants of passive Na+ and K+ permeability were determined in each patient and control and also in six parents. The results show that in Bartter syndrome, there is a significant increase in the rate constant of passive Na+ permeability without any change in passive K+ permeability. This increase in the rate constant of passive permeability might explain at least partially the increased intracellular Na+ concentration also found in these patients. Moreover, the maximal rate of ouabain sensitive Na+ efflux was increased slightly, and co-transport fluxes were variable. Parents of patients had normal erythrocyte fluxes.
Net Na+ and K+ fluxes were measured in Na+-Ioaded and K-depleted erythrocytes of three varieties of genetically hypertensive rats. In Okamoto spontaneously hypertensive rats (4 and 10-12 weeks of age), Na+ extrusion was reduced as compared to normotensive controls (Wistar/Kyoto). Na+ extrusion was also reduced in the hypertension-prone substrain of the Hebrew University Sabra rats as compared to the Na+-resistant substrain. K+ fluxes were similar in both groups. In both Okamoto spontaneously hypertensive rats and the hypertension-prone substrain, hypertension was severe and developed rapidly. An abnormally low ratio of Na+/K+ net fluxes in Na+-loaded/K+-depleted erythrocytes of human essential hypertensives was recently demonstrated (7). The absence of this abnormality in normotensive families, as in true secondary hypertension, and its presence in some young normotensives born of hypertensive parents led us to suggest that it could be an inherited character related to hypertension.In order to test this hypothesis, an investigation of net Na+ and K+ fluxes has been undertaken in three representative strains of genetically hypertensive rats, the Okamoto strain, the Lyon variety, and the hypertension-prone substrain derived from the Hebrew University Sabra rats.MATERIALS AND METHODS Rats. Male rats were used throughout this study. Okamoto spontaneously hypertensive rats (SHR) (1) and the Wistar/ Kyoto normotensive controls (WK) derived from the NIH stock were supplied by Iffa-Credo (Les Oncins, France). They were studied at 4 and 10-12 weeks of age. Systolic arterial blood pressure was recorded by tail plethysmography. Values (mm Hg; 1 mm Hg = 133 Pa) (mean i SEM) were as follows: at 4 weeks, SHR = 135 4 (n = 8), controls = 123 3 (n = 9); at 10-12 weeks, SHR = 192 + 4 (n = 9), controls = 137 + 4 (n = 10).Rats belonging to the 18th generation of the Lyon hypertensive (LHS) and normotensive (LNS) strains were isolated by selective inbreeding of a CFE albino strain derived from Sprague-Dawley (Iffa-Credo) (4). They were studied at 10 weeks of age, their systolic blood pressure being: LHS = 147 t 6 (n = 7) and LNS = 120 + 4 (n = 8); the difference between the two values was statistically significant (P < 0.001). Hypertension-prone (H) and sodium-resistant (N) rats were derived from the Hebrew University Sabra rats. The two substrains were obtained by brother-sister inbreeding and selected according to their respective sensitivity or resistance to deoxycorticosterone acetate/Na+-induced hypertension (6). They were studied at 15 weeks of age.
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