Dopamine preferentially stimulates postsynaptic α 2-adrenoceptors in the femoral vascular bed, but α 1-adrenoceptors in the renal vascular bed of the anaesthetised dog

The decrease in blood flow in response to dopamine (DA) injected intraarterially (i.a.) into the femoral or renal vascular beds was examined in the anaesthetised dog. DA or noradrenaline (NA) were 10 times more potent as vasoconstrictor agents in the femoral than in the renal vasculature. In the femolar bed, the DA induced vasoconstriction was completely resistant to antagonism by prazosin (30–300 μg/kg i.v.), but was dose-dependently blocked by the α 2-receptor antagonist idazoxan (30–300 μg/kg i.v.). In the renal bed the vasoconstrictor effects DA were resistant to blockade by idazoxan, but were prazosin sensitive indicating that α 1-adrenoceptors were involved in this response. The α-receptor agonist profile for DA was not modified in the femoral bed after blockade of dilatory D 1-receptors with SCH 23390 (0.5 mg/kg i.v. and 0.1 mg/kg per h i.v.). However, this antagonist significantly increased the vasoconstrictor potency for DA in the renal bed. The decrease in femoral blod flow induced by an injection of DA, appears to be mediated by α 2-adrenoceptors. In the renal vascular bed where the predominant α-adrenoceptor corresponds to the α 1-subtype and there are few postsynaptic α 2-receptors subserving vasoconstriction, DA can stimulate α 1-receptors but this action requires higher doses of agonist than those needed for α 2-adrenoceptor stimulation.