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There is now a considerable body of evidence to suggest that the fat cells that surround blood vessels (perivascular adipose tissue, PVAT) can influence profoundly arterial tone by releasing vasodilator adipokines which can act locally in a paracrine fashion. In healthy lean individuals the primary vasodilator released appears to be adiponectin and there is a complex interation between autonomic nerve firing in PVAT and the release of nitric oxide from adipocytes and an increased bioavailability of adiponectin. However the vasodilators that are released appear to be agonist dependent and adiponectin is certainly increased as a result of sympathomimetic stimulation. Primarily our work has focused on the role of sympathetic nerves running through PVAT and innovating adipocytes and releasing adiponectin. Electrical field stimulation studies have demonstrated clearly the release of adiponectin and the induction of relaxation which is abolished using 6-hydroxydopamine or tetrodotoxin to destroy the autonomic nerve fibres. In obesity there is evidence of beta-3 receptors on adipocytes and the loss of vasodilator activity which is clearly observed. In some models of obesity there is also evidence of an increase in vasoconstrictor prostaglandin bioavailability and increased contractility. This loss of balance between vasodilatation and vasoconstriction will lead to an increase in peripheral resistance which will decrease glucose uptake in skeletal muscle and bring about a rise in blood pressure: key components of the metabolic syndrome. Caloric restriction or weight reducing surgery can restore completely normal PVAT structure and function and this is seen even when individuals remain morbidly obese.

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