The possible role of Na+ in the development of hypertension in rats was explored in measurements of intracellular Na+, 22Na efflux, and 3H-ouabain binding sites in resistance vessels and skeletal muscles. In resistance vessels obtained from 13-week-old spontaneously hypertensive rats (SHR) or age-matched Wistar-Kyoto rats (WKY), (Na)i, total or ouabain-resistant 22Na efflux, and the concentration of 3H-ouabain binding sites showed no significant differences. Soleus muscles obtained from 6-week-old and 13-week-old SHR contained 5 to 11% more 3H-ouabain binding sites than those of WKY. The small difference in ouabain binding probably was related more to variations in growth rate and strain than to the hypertension. In SHR and WKY the Na+ and K+ contents of gastrocnemius muscles were almost identical at 6 and 13 weeks of age. By contrast, in Wistar rats in which the (Na)i of skeletal muscle was increased sixfold by K+ depletion, the systolic blood pressure was decreased by 10%. The K+ depletion was associated with a 35 to 55% decrease in the concentration of 3H-ouabain binding sites in both resistance vessels and skeletal muscles. The results provide no support for any simple cause-effect relationships between either elevated (Na)i or altered concentration of 3H-ouabain binding sites and hypertension in SHR.
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