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The role of α-adrenoceptor subtypes mediating vasoconstriction of large epicardial and small resistive coronary arteries was investigated in 26 open-chest dogs. The left circumflex coronary artery was perfused at a constant pressure. Large vessel vasomotion was determined by measurement of circumflex coronary arterial diameter (ultrasonic transit-time technique); the vasomotion of the small resistive coronary arteries was determined from calculated end-diastolic circumflex artery resistance. β-Receptors were blocked by propranolol (2 mg/kg i.v.) and both vagal nerves were cut. In eight dogs, the intracoronary administration of the α1-adrenoceptor agonist methoxamine (500 μg) increased calculated large vessel resistance by 18.8 ± 5.7% and end-diastolic resistance by 9.5 ± 0.3%. Intracoronary administration of the α2-adrenoceptor agonist BHT 920 (500 μg) did not affect large vessel resistance, but increased end-diastolic resistance by 37.5 ± 5.6%. In an additional 18 dogs, left cardiac sympathetic nerve stimulation induced an increase in large vessel resistance by 11.1 ± 0.9% and in end-diastolic resistance by 31.8 ± 3.0%. The increase in large vessel resistance was prevented by the α1-adrenoceptor antagonist prazosin (1.2 mg/kg i.v.), which still permitted an increase in end-diastolic resistance by 23.0 ± 3.2%. The increase in end-diastolic resistance was prevented by the α2-adrenoceptor antagonist rauwolscine (0.2 mg/kg i.v.), which still permitted an increase in large vessel resistance by 11.9 ± 2.4%. The calcium antagonist nifedipine (20 μg/kg i.v.) prevented both the increase in large vessel resistance and end-diastolic resistance during sympathetic stimulation. Our experiments indicate that α-adrenoceptor-mediated vasoconstriction of large coronary arteries is mediated exclusively by α1-adrenoceptors, whereas α-adrenergic vasoconstriction of small resistive coronary arteries is mediated in part by α1-, but predominantly by α2-adrenoceptors. The calcium antagonist nifedipine can antagonize the vasoconstriction initiated by α1- as well as by α2-adrenoceptors.