White adipocytes surround almost all blood vessels in the human body. It was thought previously that these cells merely provide mechanical support for the adjacent small vessels and are little more than fat storage units. Recent studies have identified these cells as metabolic and vasoactive engines that produce and secrete molecules that can affect the function of their adjacent small vessels. The adipocytes and a number of other cell types (including inflammatory cells) surrounding the vessels are collectively termed the PeriVascular Adipose Tissue (PVAT). Work from our group has shown previously that, in health, PVAT conveys a vasorelaxant effect on adjacent small arteries and that this effect is not observed in obesity thus the vessels must exist at an elevated level of basal tone. It is plausible that increased basal vessel constriction can explain the elevated blood pressure amongst the obese population and a better understanding of the obesity-induced PVAT damage may lead to clues to a new approach in the treatment of the condition which burdens its sufferers with a greater cardivascular risk profile. In this thesis we have studied individuals with morbid obesity at baseline and six months following surgery and observed that PVAT function following dramatic weight loss restores the PVAT vasorelaxant effect close to that observed in lean patients. Moreover, we have concluded that inflammation plays a significant role in this process and indeed using protocols with antioxidant enzymes we were able to restore the damaged PVAT function at baseline. We have have shown also that in health, PVAT vasorelaxant function is independent of the endothelium, and that obesity-induced PVAT damage and its reversal following weight loss and ex-vivo anti-oxidant treatment are both independent of the endothelium and at least in part due to nitric oxide bioavailability. Finally, we have observed that in sleep apnoea, which often coexists with morbid obesity and hypertension, there is a greater degree of PVAT inflammation.