Objectives: 

Excess visceral adiposity is associated with cardiovascular disease. The SHROB rat is a model of metabolic syndrome with visceral obesity. We have reported that mesenteric resistance arteries (MRA) of SHROB suffer a severe endothelial dysfunction. Our present aims are to determine whether visceral fat surrounding these vessels underlies this endothelial dysfunction, and if so, whether this is due to disruption of the endothelial NO pathway. Also, to determine whether vasoactive adipokines such as angiotensin II, endothelin-1, prostaglandin E2, prostacyclin, thromboxane A2 or ROS contribute to the mentioned endothelial dysfunction.

Materials: 

We have measured changes in isometric tension developed by segments of MRA from SHROB and control WKY rats in 2 different conditions: a) maintaining a sphere of perivascular adipose tissue (PAT group), or b) completely dissecting adventitial tissue (without PAT group). Endothelial function was assessed by dose-response curves to acetylcholine.

Results: 

Arteries with PAT from SHROB (but not those from WKY) relax much worse than those without PAT. Inhibition of NO synthase activity decreased the responses to acetylcholine in all groups (i.e.: SHROB without PAT, WKY with PAT and WKY without PAT) except in the SHROB with PAT group. Inhibition or blockade of angiotensin II, endothelin-1, cyclooxygenase II, prostacyclin or thromboxane A2 improved to different extents the responses to acetylcholine of SHROB with PAT arteries. However, relaxation of WKY with PAT arteries improved only by inhibiting cyclooxygenase II or blocking prostaglandin E2 receptors.

Conclusions: 

Visceral PAT of SHROB, but not that of WKY, releases adipokines that impair endothelial function of adjacent resistance arteries by altering the NO pathway. Adipose tissue is a source of vasoactive prostaglandins, both in mesenteric fat from non-obese and obese rats. However, in the latter, the nature of the adipocytic prostaglandins contribute to the endothelial dysfunction of their MRA.