Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo.

The role of alpha-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. beta-Receptors were blocked by propranolol (2 mg/kg i.v.) and both vagal nerves were cut. In eight dogs, the intracoronary administration of the alpha 1-adrenoceptor agonist methoxamine (500 micrograms) increased calculated large vessel resistance by 18.8 +/- 5.7% and end-diastolic resistance by 9.5 +/- 0.3%. Intracoronary administration of the alpha 2-adrenoceptor agonist BHT 920 (500 micrograms) 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 alpha 1-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 alpha 2-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 micrograms/kg i.v.) prevented both the increase in large vessel resistance and end-diastolic resistance during sympathetic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)