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(Circulation. 2004;109:664-670.)
© 2004 American Heart Association, Inc.

Basic Science Reports

Exercise Training Enhances Vasodilation Responses to Vascular Endothelial Growth Factor in Porcine Coronary Arterioles Exposed to Chronic Coronary Occlusion

Jennifer A. Fogarty, PhD; Judy M. Muller-Delp, PhD; Michael D. Delp, PhD; Mildred L. Mattox, BS; M. Harold Laughlin, PhD; Janet L. Parker, PhD

From the Cardiovascular Research Institute and Department of Medical Physiology, Texas A&M University System Health Science Center (J.A.F., M.L.M., J.L.P.), and Department of Health and Kinesiology (J.M.M.-D., M.D.D.), Texas A&M University, College Station, Tex, and Dalton Cardiovascular Research Center and Departments of Physiology and Biomedical Sciences, University of Missouri, Columbia (M.H.L.).

Correspondence to Janet L. Parker, Cardiovascular Research Institute and Department of Medical Physiology, TAMUS HSC MS 1114, College Station, TX 77843-1114. E-mail jlp{at}tamu.edu

Received December 30, 2002; de novo received May 9, 2003; revision received October 3, 2003; accepted October 6, 2003.

Background— Chronic coronary occlusion (CCO) impairs endothelial function of distal collateral–dependent microvasculature; however, long-term exercise training (EX) seems to improve endothelial dysfunction. We hypothesized that EX enhances vasodilation responses to vascular endothelial growth factor (VEGF₁₆₅), mediated via nitric oxide (NO), in arterioles exposed to CCO.

Methods and Results— The proximal left circumflex coronary artery (LCx) of female Yucatan miniswine was surgically instrumented with an ameroid occluder to induce CCO; 8 weeks after surgery, animals were randomized into 14-week sedentary (SED) or EX (treadmill; 5 d/wk) protocols. Coronary arterioles (100 µm in diameter) were isolated from collateral-dependent (LCx) and nonoccluded (left anterior descending; LAD) perfused myocardium of SED and EX animals. Vasodilation was assessed by videomicroscopy and MacLab data acquisition. Responses to VEGF₁₆₅ were unaffected by EX in nonoccluded LAD arterioles; in contrast, EX markedly enhanced VEGF₁₆₅-induced vasodilation of collateral-dependent LCx arterioles (P<0.05; EX versus SED). Furthermore, VEGF₁₆₅-induced vasodilation of EX LCx arterioles exceeded that of EX or SED LAD arterioles (P<0.05). Enhanced vasodilation of EX LCx arterioles was abolished by inhibition of NO synthase and tyrosine kinase activity. Combined inhibition of NO synthase and cyclooxygenase decreased VEGF₁₆₅-induced vasodilation of all vessels.

Conclusions— EX enhances VEGF₁₆₅-induced vasodilation in arterioles distal to CCO; EX effects seem to be mediated through increases in NO.

Key Words: microcirculation • nitric oxide • occlusion • coronary disease • collateral circulation

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