Vasodilatation and modulation of vasoconstriction in canine subcutaneous adipose tissue caused by activation of β‐adrenoceptors

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Abstract
The present experiments were undertaken to study the balance between vascular α‐ and β‐adrenoceptors in canine subcutaneous adipose tissue during sympathetic nerve stimulation and noradrenaline injections. Propranolol potentiated and prolonged the vasoconstrictor response to close i.a. injections of noradrenaline. The vasoconstriction induced by brief nerve stimulation (0.5 to 8 Hz) was, however, unaltered by the β‐adrenoceptor blockade. During prolonged nerve stimulation the vasoconstrictor response was well maintained at 1.5 Hz but at 4 Hz there was a gradual escape. The escape phenomenon at 4 Hz was diminished by propranolol. The β1‐selective antagonist practolol, like propranolol, potentiated and prolonged the vasoconstriction induced by noradrenaline injections and reduced the vasoconstrictor escape during prolonged nerve stimulation at 4 Hz. Furthermore, the vasodilatation induced by noradrenaline injection or nerve stimulation during α‐adrenoceptor blockade was diminished by practolol. Practolol also blocked the lipolytic response to noradrenaiine and nerve stimulation. The β2‐selective antagonist H35/25 blocked the effects of the β2‐selective agonist salbutamol but failed to alter noradrenaline as well as nerve stimulation induced vascular and lipolytic β‐adrenoceptor responses. The present results provide further support for the hypothesis that vascular β‐adrenoceptors in adipose tissue are humoral (noninnervated), preferentially activated by circulating noradrenaline. Moreover, both vascular and lipolytic β‐adrenoceptors activated by noradrenaline in adipose tissue are best classified as β1‐adrenoceptors.