Platelet sodium kinetics, blood pressure and serum urate: aberrations in non-obese men at risk for type 2 diabetes mellitus.

The rate constants for the ouabain- and frusemide-sensitive 22Na+ efflux, the number of [3H]ouabain binding sites and the effect of plasma on [3H]ouabain binding were determined in platelets, as were blood pressure (BP) and serum urate concentrations, in 35 normoglycaemic men with family histories of type 2 diabetes (hereditary group), in 18 subjects with impaired glucose tolerance (IGT) and in 28 normoglycaemic controls. All subjects were non-obese males of comparable age. Earlier findings of increased BP both in normoglycaemic subjects with family histories of type 2 diabetes and in IGT subjects were confirmed. The mean serum urate concentration was significantly higher in the hereditary group than in controls, and intermediate in IGT subjects. The ouabain-sensitive 22Na+ efflux rate constant was significantly decreased in IGT subjects without any concomitant change in the number of [3H]ouabain binding sites. No differences in any of the rate constants for 22Na+ efflux, or in the number of [3H]ouabain binding sites, were noted between the hereditary group and controls. The ability of deproteinized plasma samples to interfere with [3H]ouabain binding to test platelets from one healthy individual was similar in all three groups. The present findings are not consistent with the hypothesis that the BP increase in normoglycaemic subjects with family histories of type 2 diabetes is linked to a disturbance in sodium transport. Our data suggest a decreased Na+/K+-ATPase activity in IGT, which may be of pathophysiological significance in relation to hypertension.