Perivascular adipose tissue (PVAT) has been proposed as a cause of atherosclerosis, recently. The location of PVAT is in association with the artery wall, which enables diffusion of adipokines (e.g. superoxide anion, angiotensin II, tumor necrosis factor-α, and adiponectin). The adipokines are capable of inducing endothelial dysfunction and enhancing vasoconstriction in rat thoracic aortas. Caveolin-1 (Cav-1), a structure protein of caveolae, is present in most of cells involved in the development of atherosclerosis. Cav-1 inhibits nitric oxide (NO) production by occupying the calcium/calmodulin binding site of endothelial NO synthase. The inhibition of NO production is a characteristic of endothelial dysfunction. In this study, adult male Wistar rats weighing 265 to 305 g were euthanatized by intravenous injection of overdose of sodium pentobarbital. The thoracic aortas were isolated, dissected without the PVAT, divided into endothelium-intact (+E) and endothelium-denuded (-E) groups, and mounted in organ bath containing a Krebs’ solution bubbled with 95% O2 and 5% CO2 at 37 C. PVAT was incubated in Krebs’ solution for 30 minutes and transferred to organ bath before the isometric tension studies. The remaining aortas were frozen for Western blotting. The dose-response curve of phenylephrine, acetylcholine, and sodium nitroprusside were performed to examine the vascular reactivity and endothelial function, respectively. We found that the unknown factor(s) released from PVAT increased Cav-1 protein expression and induced a vasocontractile effect via inhibition of endothelial NO production in rat thoracic aorta.