Abstract MP08: Perivascular Adipose Tissue Reduces Acetylcholine Relaxation In Femoral Artery From Obese Mice
Obesity causes serious metabolic derangements and is closely related to high risk of cardiovascular disease. The role of perivascular adipose tissue in vascular function has recently been recognized. The aim of this study was to investigate the role of perivascular adipose tissue in the vascular responsiveness of femoral artery in obese mice. Male mice (C57BL6/JUnib; body weight: 20.5±0.5) were divided into: control (CT, n=5) and obese (OB, n=5). During 16 weeks the CT mice were fed with standard chow and to induce obesity the OB mice were fed with high fat diet. Concentration-response curves to acetylcholine (ACh), sodium nitroprusside (SNP), phenylephrine (PHE) and thromboxane A2 analog (A2) were obtained in femoral arteries in the absence (PVAT-) or presence (PVAT+) of perivascular adipose tissue. The potency (pEC50) and maximal responses (EMAX) were calculated. The glycaemia and serum total cholesterol were measured. As expected, in OB group the body weight (46±0.9 g), epididymal fat pad (1.4±0.07 g), glycaemia (157±9 mg/dl) and total cholesterol (226±45 mg dl) were increased when compared to CT (28±1 g, 0.3±0.03 g, 98±0.5 mg/dl and 80±4 mg/dl; respectively). The amount of perivascular adipose tissue in femoral rings was markedly increased in OB (2.83±0.64 mg/mm) when compared to CT (0.14±0.02 mg/mm). The PVAT+ did not modify the relaxation response to ACh in CT group. However in OB mice the rings PVAT+ showed a reduction in pEC50 (PVAT+:6.58+0.2 and PVAT-:7.24±0.1; approximately 4.6 fold) and in EMAX to ACh. The relaxation responses to NO donor, SNP, were not modified in all groups. The PVAT+ did not change the response to PHE in all groups. Interestingly in OB group the EMAX to PHE was increased when compared to CT, in rings PVAT- and PVAT+. Neither the pEC50 nor EMAX were modified to U46619 in all groups. In conclusion, the presence of perivascular adipose tissue causes endothelial dysfunction in femoral artery from obese mice.
Author Disclosures: A.C.S. Sponton: None. A.S. Sousa: None. C.B. Trifone: None. M.A. Delbin: B. Research Grant (includes principal investigator, collaborator, or consultant and pending grants as well as grants already received); Significant; FAPESP 2013/02960-1.
- © 2014 by American Heart Association, Inc.