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Perivascular Fat Alters Reactivity of Coronary Artery: Effects of Diet and Exercise


Medicine & Science in Sports & Exercise: December 2007 - Volume 39 - Issue 12 - p 2125-2134
doi: 10.1249/mss.0b013e318156e9df
BASIC SCIENCES: Original Investigations

ABSTRACT Perivascular adipose tissue (PAT) has been reported to blunt agonist-induced arterial tone via a relaxing factor acting in a paracrine manner.

The purpose of this study was to test the hypothesis that PAT of porcine coronary artery blunts constriction similarly and that this anticontractile effect of PAT is altered by diet and/or exercise training.

Methods: Fourteen adult male pigs were fed a normal-fat (NF) diet, and 10 adult male pigs were fed a high-fat/cholesterol (HF) diet. Four weeks after the initiation of diet, pigs were exercised (EX) or remained sedentary (SED) for 16 wk, yielding four groups: 1) NF-SED, 2) NF-EX, 3) HF-SED, and 4) HF-EX. Left circumflex coronary artery (LCX) rings were prepared with PAT left intact or removed. LCX reactivity to acetylcholine (ACh), endothelin (ET-1), bradykinin (BK), and sodium nitroprusside (SNP) was assessed in vitro using standard techniques.

Results: The results demonstrate that both ACh and ET-1 elicited dose-dependent increases in tension from LCX rings from all groups. Removal of PAT had no significant effect on ACh-induced contractions in any group. In contrast, removal of PAT increased ET-1-induced tension in LCX from NF-SED, HF-SED, and HF-EX but not NF-EX. PAT had no significant effect on relaxation responses to BK except in HF-EX animals, where removal of PAT increased BK-induced relaxation. PAT removal decreased SNP-induced relaxation in HF-LCX, but not LCX from NF pigs, suggesting basal release of a relaxing factor LCX from HF pigs.

Conclusion: PAT blunts contractions induced by ET-1 in LCX from NF and HF pigs. Whereas EX abolished this effect of PAT in NF pigs, exercise did not alter the anticontractile effect in HF pigs.

1Department of Medical Pharmacology and Physiology, 2Department of Biomedical Sciences, and 3Dalton Cardiovascular Research Center, College of Veterinary Medicine, University of Missouri, Columbia, MO

Address for correspondence: M. H. Laughlin, Ph.D., University of Missouri, Department of Biomedical Sciences, 1600 E. Rollins, E102 Vet Med Bldg, Columbia, MO 65211; E-mail:

Submitted for publication April 2007.

Accepted for publication July 2007.

©2007The American College of Sports Medicine