The role of neuronal uptake at?- and?-adrenoceptor sites in subcutaneous adipose tissue

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Abstract
Intravascular noradrenaline infusion may cause vasodilatation or vasoconstriction in subcutaneous adipose tissue, whereas sympathetic nerve activity causes vasoconstriction only. This discrepancy may be due to a differential distribution of α- and β-adrenoceptors in relation to adrenergic nerve terminals in the adipose tissue vessels. In order to test this hypothesis the extent of prejunctional supersensitivity to noradrenaline was studied after blockade the neuronal uptake of noradrenaline with cocaine. In the autoperfused, isolated inguinal canine adipose tissue pretreatment with cocaine (200–600 μg close i.a.) increased lipolysis following sympathetic nerve stimulation or close i.a. injection of noradrenaline. Cocaine also potentiated the vasoconstriction induced by nerve stimulation (1–3 Hz) or intra-arterial noradrenaline (0.2–2 nmoles) as well as the vasodilatation induced by sympathetic nerve stimulation (1–3 Hz) after α-receptor blockade. However, the vasodilatation following close i.a. injection of noradrenaline after α-receptor blockade was not changed by cocaine. The results indicate that the functionally important vascular α-adrenoceptors in adipose tissue are in close contact with adrenergic nerve terminals, whereas most vascular β-adrenoceptors seem to be unrelated to the nerve terminals. Thus, the α-adrenoceptors in the adipose tissue vessels may be classified as innervated receptors, in contrast to the vascular β-adrenoceptors which may be more acessible to circulating catecholamines and may be classified as humoral receptors. Furthermore at least some of the β-receptors on the adipocytes seem to be located close to sympathetic nerve terminals.