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J Appl Physiol 87: 1948-1956, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 5, 1948-1956, November 1999

Exercise training improves endothelium-mediated vasorelaxation after chronic coronary occlusion

Kawanza L. Griffin1,2, M. Harold Laughlin1,2,3, and Janet L. Parker1,2,4

1 Dalton Cardiovascular Research Center and 2 Departments of Physiology and 3 Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211; and 4 Department of Medical Physiology, Texas A & M University, College Station, Texas 77843

The present study evaluated combined effects of chronic coronary occlusion and exercise training on endothelial function. Gradual occlusion was produced by placement of an ameroid constrictor around the proximal left circumflex (LCX) coronary artery of female swine. Two months after placement of the ameroid, animals were restricted to their pens or exercise trained for 16 wk. Epicardial arteries (>500 µm ID) were isolated from the collateral-dependent LCX coronary artery distal to the occlusion and the nonoccluded left anterior descending (LAD) coronary artery. Bradykinin- and ADP-mediated relaxation of LCX and LAD coronary arteries was enhanced after exercise training. Inhibition of nitric oxide synthase with NG-nitro-L-arginine methyl ester decreased bradykinin- and ADP-mediated relaxation in LCX and LAD myocardial regions. Importantly, combined inhibition of effects of endothelium-derived hyperpolarizing factor with increased extracellular K+ (20-30 mM) and nitric oxide synthase completely abolished coronary LAD and LCX relaxation to bradykinin. Our data indicate that exercise training improves endothelium-mediated relaxation of arteries isolated after chronic coronary artery occlusion, likely as a result of enhanced production of nitric oxide and endothelium-derived hyperpolarizing factor.

bradykinin; collateral circulation; vasodilation


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