The role of α₁- and α₂-adrenoceptors in the coronary vasoconstrictor responses to neuronally released and exogenous noradrenaline in the dog

Summary

1. Coronary vasoconstriction was examined in response to the neuronal release of noradrenaline produced by bilateral carotid occlusion and the infusion of tyramine (5 – 50 Erg/kg/min i. v.) in anaesthetized dogs which had been vagotomized and treated with the β-adrenoceptor antagonist propranolol (1.0 mg/kg i. v.). These responses were compared to those produced by the infusion of noradrenaline (0.1 – 0.5 μg/kg/min i. v.). 2. Similar increases in late diastolic coronary resistance were produced by bilateral carotid occlusion (0.70 ± 0.25 mmHg min/ml), and intravenous infusions of tyramine, 20 μg/kg/min (0.70 ± 0.12 mm Hg min/ml) and noradrenaline, 0.5 gg/kg/min (0.59 ± 0.11 mm Hg min/ml). 3. Selective antagonism at α₁-adrenoceptors with prazosin (0.5 mg/kg i. v.) attenuated the coronary constrictor response to bilateral carotid occlusion (0.36 ± 0.09 mm Hg min/ml), tyramine (0.12 ± 0.06 mm Hg min/ml) and noradrenaline (0.18 ± 0.07 mm Hg min/ml). Antagonism at α₂-adrenoceptors with idazoxan (1 mg/kg i. v.) attenuated the coronary vasoconstriction produced by bilateral carotid occlusion (0.30 ± 0.06 mmHg min/ml), tyramine (0.17 ± 0.08 mmHg min/ml) and noradrenaline (0.12 ± 0.03 mm Hg min/ml). Combined antagonism at both α₁- and α₂-adrenoceptors with prazosin and idazoxan abolished the responses to bilateral carotid occlusion, tyramine and noradrenaline. 4. These results show that coronary vasoconstriction produced by either neuronally released or exogenous noradrenaline is mediated by both α₁ and α₁-adrenoceptors. It appears that in the coronary resistance vessels of the dog postjunctional α₁- and α₂-adrenoceptors are both innervated by sympathetic nerves.