| dc.description.abstract | Abstract
Adipose tissue is presently considered to be an active endocrine and paracrine organ. Obesity is closely related with several disorders including hypertension. Obese seem to have a dysfunctional adipose tissue, which shows an ongoing inflammation, and the production of cytokines regulating inflammation as well as more specific adipokines are changed. Also an elevated activity of 11β-HSD-1 is seen in these patients. Perivascular fat has been shown to attenuate vascular responsiveness. Our study aims to investigate if inflammation, specifically corticosterone, in adipose tissue changes the vasodilatory effect of perivascular fat.
Mesenteric small arteries from adult, female, Sprague-Dawley rats were isolated and mounted in a Mulvany-Halpern myograph. Perivascular fat was initially removed from all vessels and their noradrenaline sensitivity determined. Next perivascular fat was wrapped around every other vessel followed by a new determination of their noradrenaline sensitivity. Finally the noradrenaline sensitivity was determined after previous addition of corticosterone (10 µM).
In accordance with previous reports we found that addition of fat around the vessels caused a significant reduction in noradrenaline sensitivity (∆log EC50 -0,369± 0.083, n=10) and a reduction in maximal response (-10,7%± 2,45). Addition of corticosterone partially anatagonised the vasodilatory effect of perivascular fat. The noradrenaline sensitivity tended to increase (∆log EC50 0.182± 0.110, n=8) in vessels with fat and corticosterone compared with vessels with fat, but no corticosterone present. There was no effect on vascular responsivness in vessels without perivascular fat before and after addition of corticosterone.
These data suggest that corticosterone may modulate the vasodilatory effect of perivascular fat. | sv |
