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Forty 11-week-old Dahl salt-sensitive rats were divided into four groups matched for blood pressure and weight. Croup I was given a sodium-deficient diet, group II a sodium-enriched diet, group III a sodium-enriched diet plus a calcium supplement and group IV a sodium-enriched diet plus nitrendipine, a calcium antagonist. For the first 18 weeks, when the sodium-enriched diet contained 2.6% sodium, there were no differences in blood pressure between the groups; the sodium content was then increased to 8%, and the diets continued for 12 more weeks. At 41 weeks old, the rats in group II had significantly ( p <0.05) higher systolic blood pressures than the other groups. Erythrocytes from the rats on the low-sodium diet had significantly (P<0.025) lower intracellular sodium (3.9 ± 0.4mmol/l) while cells from the rats given nitrendipine had significantly (p <0.005) higher intracellular sodium (13.3 ± 0.8mmol/l) than those from the rats on a high-salt diet (7.4 ± 1.4mmol/l). Nitrendipine caused significant (p <0.05) decreases in both ouabain-sensitive and furosemide-sensitive sodium efflux. Platelet aggregation in response to 2 |imol/l adenosine diphosphate was not significantly affected by the nitrendipine. The evidence that nitrendipine markedly affects sodium transport supports the hypothesis that an interaction of calcium and sodium may be involved in blood pressure control.