Coronary vasoconstriction mediated by α₁- and α₂-adrenoceptors in conscious dogs

Coronary vasoconstriction was examined in response to the selective stimulation of α₁- and α₂-adrenoceptors in chronically instrumented conscious dogs. Norepinephrine (NE, 0.05 and 0.1 μg·kg^-1·min^-1), a mixed α₁- to α₂-adrenoceptor agonist, phenylephrine (PE, 0.5 and 1.0 μg·kg^-1·min^-1), a preferential α₁-adrenoceptor agonist, and B-HT 920 (1.0 μg·kg^-1·min^-1), a preferential α₂-adrenoceptor agonist, were infused intravenously after ganglionic (hexamethonium, 30 mg/kg iv), β-adrenoceptor (propranolol, 1.0 mg/kg iv), and muscarinic receptor (atropine methylbromide, 0.1 mg/kg iv) antagonism. Equipressor doses of the α-adrenoceptor agonists caused similar increases in calculated late diastolic coronary resistance (NE, 0.57 ± 0.10 mmHg·ml^-1·min; PE, 0.61 ± 0.13 mmHg·ml^-1·min; B-HT 920, 0.64 ± 0.09 mmHg·ml^-1·min). Mechanically increasing aortic root pressure to levels similar to those observed in response to α-adrenoceptor stimulation did not increase coronary resistance. Preferential antagonism of α₁-adrenoceptors with prazosin (1 mg/kg iv) abolished the vasoconstrictor response to PE but had a lesser effect on the response to B-HT 920. Antagonism of α₂-adrenoceptors with rauwolscine (α-yohimbine, 0.1 mg/kg iv) abolished the vasoconstrictor response to B-HT 920 but had a lesser effect on the response to PE. The response to NE was reduced to a similar degree by either α₁- or α₂-adrenoceptor antagonism. These results demonstrate that stimulation of both α₁- and α₂-adrenoceptors causes constriction of the coronary resistance vessels in the conscious dog. The coronary vasoconstrictor response to NE is mediated by both α-adrenoceptor subtypes.