Potassium supplementation attenuates experimental hypertensive renal injury.

The long-term roles of dietary sodium and potassium on the renal end-organ damage of hypertension were investigated in Wistar-Kyoto (WKY) and in spontaneously hypertensive (SHR) rats. Eight rats from each strain were maintained since I month of age on one of four dietary combinations of either low (0.4%) or high (6.0%) NaCI and low (0.51%) or high (7.6%) KCI providing sodium/potassium molar ratios of 1:1, 1:15, 15:1, and 15:15, respectively. Urinary sodium/potassium excretion ratios confirmed the proportion of salts consumed. Systolic blood pressures (SBP) were similar at 5 months of age and at the completion of the study at 9.5 months; SBPwas significantly higher in SHRthan in WKY rats and was not attenuated by dietary potassium supplementation of a magnitude that raised plasma potassium concentrations. Albumin excretion rate (AER) was also higher in SHRthan in WKY rats (P < 0.0001). In SHR, AER rose further with high sodium intake (P < 0.035) but, contrary to SBP,was ameliorated by an equimolar addition of potassium (P< 0.01). Morphologic lesions were generally absent in WKY rats and were more common in SHRas a group (P< 0.001). In all four SHRgroups, the graded histopathologic injury correlated well with measured AER but a major improvement in hypertensive renal lesions occurred largely in the KCI-supplemented, salt-loaded SHR group. These results show a disassociation between the effects of dietary monovalent cations on the level of SBPand their effect on renal injury. Sodium aggra