The pharmacodynamic properties of a beta-blocker are mainly determined by its affinity to beta1 and beta2-receptors respectively and by its intrinsic activity. It is suggested that there is no absolute organ separation of the two receptor sub-types. Instead both beta1 and beta2-receptors are involved in the mediation of the same effect. The frequency distribution ratio of beta1/beta2-receptors varied markedly among various effector responses. A non-selective and a beta1-selective blocker may have different haemodynamic effects when the levels of circulating adrenaline are high, because of their markedly different potency in inhibiting the beta2-mediated vasodilator effect of adrenaline. Data are presented which suggest the existence of a presynaptic beta1-receptor mediating a positive feedback mechanism on neuronal release of noradrenaline.