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Cardiac sympathetic nerve stimulation (CSNS) can induce vasoconstriction distal to severe coronary stenoses by activation of vascular α2-adrenoceptors. Whether nifedipine can antagonize this CSNS-induced vasoconstriction was tested in 11 anesthetized, vagotomized dogs. CSNS decreased the end-diastolic resistance of intact coronary arteries from 0.76 ± 0.07 to 0.56 ± 0.05 mm Hg · min · 100 g/ml (p < 0.05). In contrast, the resistance distal to severe stenoses, which were defined by a reduction of the postocclusive reactive hyperemia to almost zero, was increased during CSNS from 0.52 ± 0.06 to 0.87 ± 0.14 mm Hg · min · 100 g/ml (p < 0.05). This increase in resistance was associated with severe ischemia, as indicated by a net lactate production of the circumflex-perfused myocardium and a decrease in systolic segment shortening from 8.4 ± 0.7 to 7.0 ± 0.7% (p < 0.05). Both intracoronary (10 μg) and intravenous (10 μg/kg) administration of nifedipine did not change the poststenotic resistance at rest, but did prevent the CSNS-induced increase in resistance, the decrease in regional contraction, and the net lactate production. We conclude that nifedipine can prevent the deleterious role of α-adrenoceptor-mediated vasoconstriction in the genesis of myocardial ischemia.