Dopexamine is an agonist at peripheral dopamine receptors and at beta 2-adrenoceptors. Dopexamine has approximately one-third the potency of dopamine in stimulating the vascular DA1-receptor in the dog, resulting in a fall in renal vascular resistance of 20% at 2.3 X 10(-8) mol kg-1 (i.a.). Prejunctional DA2-receptors are also stimulated by dopexamine, resulting in a reduction of neurogenic vasoconstriction in the rabbit isolated ear artery (IC50 of 1.15 X 10(-6)M) and of neurogenic tachycardia in the cat (ID50 of 5.4 X 10(-8) mol kg-1, i.v.), with a potency six and four times less respectively than that of dopamine. By contrast, dopexamine is approximately 60 times more potent than dopamine as an agonist at the beta 2-adrenoceptor of the guinea-pig isolated tracheal chain, with an EC50 of 1.5 X 10(-6)M. Both dopexamine and dopamine are weak agonists at the guinea-pig atrial beta 1-adrenoceptor over the concentration range 10(-7) to 10(-4) M, but dopexamine has an intrinsic activity of only 0.16 relative to dopamine. Dopexamine does not stimulate postjunctional alpha 1- or alpha 2-adrenoceptors in the canine isolated saphenous vein, whereas dopamine is an agonist, approximately 120 times less potent than noradrenaline. Unlike dopamine and salbutamol, dopexamine does not cause arrhythmias in the guinea-pig isolated perfused heart at doses of up to 10(-5) mol, which is a thousand times the minimum cardiostimulant dose. The combination of agonist properties at peripheral dopamine receptors and at beta 2-adrenoceptors, with little or no activity at alpha- and beta 1-adrenoceptors gives dopexamine a novel pharmacological profile. This may confer advantages over dopamine in the treatment of acute heart failure.