After β-adrenergic blockade, dopamine causes coronary vasoconstriction that is blocked by nonselective α-adrenergic antagonists. This study was carried out to determine the relative importance of α1- and α2-adrenoceptors in mediating coronary vasoconstriction in response to dopamine. Because dobutamine has been reported to cause α-adrenergic stimulation, the response to dobutamine was also examined. The circumflex coronary artery was cannulated and perfused at a constant blood flow rate in 14 dogs; coronary vasomotor responses were assessed from changes in perfusion pressure. Central effects were eliminated by vagotomy and stellate ganglionectomy; propranolol (1 mg/kg i.v.) was administered to block β-adrenergic effects. The coronary responses to intracoronary bolus doses of dopamine and dobutamine were determined; the effects of selective α1-blockade with prazosin (600μ.g/kg i.v.) and selective α2-blockade with idazoxan or rauwolscine (1-5 μ.g/kg per min intracoronary for 10 min) were examined. Dopamine produced dose-related coronary vasoconstriction; this response was not significantly altered by α1-blockade with prazosin, but was abolished by the addition of α2-adrenergic blockade with idazoxan or rauwolscine. Dobutamine did not produce coronary vasoconstriction at any dose tested. These data demonstrate that coronary vasoconstriction produced by dopamine is mediated through postjunctional α2-adrenergic receptors.
- Adrenergic vasoconstriction
- Coronary blood flow