THE vascular responses in adipose tissue seem to depend on whether noradrenaline (NA) is released from the sympathetic nerve terminal system or whether it is reaching the receptors by means of the vasculature. Thus electric stimulation of adrenergic nerves to adipose tissue invariably causes α-receptor-mediated vasoconstriction, whereas infusion of NA intravascularly may induce β-receptor-mediated vasodilatation1–4. Likewise intravenous tyramine in monkeys causes vasoconstriction in adipose tissue whereas intravenous NA induces vasodilatation5. Since tyramine acts by releasing NA from the sympathetic nerve terminal system, these observations also indicate that NA produces qualitatively different effects depending on how it is delivered to the vascular adrenergic receptors. Our results indicate that the vascular adrenergic α-receptors only are located close to the adrenergic nerve terminal system, whereas the vascular β-receptors may have a different distribution, being farther away from the adrenergic nerve terminals. Consequently, the α-receptors may be affected primarily by NA released from the nerve terminals, whereas the β-receptors are primarily stimulated by circulating catecholamines.