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

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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.