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This study examines the role of calcium in contractions induced by Na+, K+ ATPase inhibition in blood vessels from spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY). Helical strips of aortae from SHR contract more rapidly in response to ouabain or potassium-free conditions than those from WKY rats. Dose-response curves to calcium in SHR aortae treated with 10-3 mol/l ouabain were shifted to the left of those in WKY. Treatment with 10-3 mol/l EGTA shifted dose-response curves to calcium in ouabain-treated strips to the left in both strains. The magnitude of the leftward shift induced by EGTA was greater in WKY aortic strips than in those from SHR. Similarly, treatment with EGTA increased the rate of contractile responses to potassium-free solution in WKY aortae to a greater extent than in SHR aortae. Verapamil (10-6 mol/l) depressed contractions induced by ouabain and potassium-free solution and abolished the differences between SHR and WKY aortae in terms of contraction rate. Calcium-free conditions completely blocked contractions caused by sodium pump inhibition. These results suggest that the difference in responsiveness to sodium pump inhibition in SHR and WKY rats results from an alteration in calcium entry through verapamil-sensitive calcium channels.