Role of pre‐ and postjunctional inhibition by prostaglandin E2 of lipolysis induced by sympathetic nerve stimulation in dog subcutaneous adipose tissue in situ

Abstract

1 Canine subcutaneous adipose tissue was isolated and autoperfused in situ after labelling of the noradrenaline stores by ³H-(—)-noradrenaline. 2 Prostaglandin E₂ (10–200 ng/ml) increased blood flow and glucose uptake, and caused a dose-dependent inhibition of lipolysis induced by sympathetic nerve stimulation (4 Hz). The actions of exogenous prostaglandin E₂ are therefore similar to those of prostaglandin E₁ in this tissue. There were no consistent effects of prostaglandin E₂ on the vasoconstriction or on the ³H-noradrenaline overflow induced by nerve stimulation. 3 Phenoxybenzamine (1·5–2 mg i.a.) caused a 5-fold increase in ³H-noradrenaline overflow and a 95% reduction of the vasoconstrictor response to nerve stimulation. The lipolytic response was similar to that of the control. Prostaglandin E₂ (100–200 ng/ml) administered after phenoxybenzamine caused a 90% inhibition of lipolysis, while the vasoconstrictor response was enhanced to about 50% of control. Prostaglandin E₂ inhibited ³H-noradrenaline overflow by about 50% but it was still larger than that of the control. 4 It is suggested that exogenous prostaglandin E₂ inhibits lipolysis induced by sympathetic nerve stimulation mainly by a postjunctional action in canine subcutaneous adipose tissue.