AHEART June 47/6

Heaps, Cristine L., Michael Sturek, Julie A. Rapps, M. Harold Laughlin, and Janet L. Parker. Exercise training restores adenosine-induced relaxation in coronary arteries distal to chronic occlusion. Am J Physiol Heart Circ Physiol 278: H1984–H1992, 2000.—We previously reported that canine collateral-dependent coronary arteries exhibit impaired relaxation to adenosine but not sodium nitroprusside. In contrast, exercise training enhances adenosine sensitivity of normal porcine coronary arteries. These results stimulated the hypothesis that chronic coronary occlusion and exercise training produce differential effects on cAMPversus cGMP-mediated relaxation. To test this hypothesis, Ameroid occluders were surgically placed around the proximal left circumflex coronary artery (LCx) of female Yucatan miniature swine 8 wk before initiating sedentary or exercise training (treadmill run, 16 wk) protocols. Relaxation to the cAMP-dependent vasodilators adenosine (1027 to 1023 M) and isoproterenol (3 3 1028 to 3 3 1025 M) were impaired in collateral-dependent LCx versus nonoccluded left anterior descending (LAD) arterial rings isolated from sedentary but not exercise-trained pigs. Furthermore, adenosine-mediated reductions in simultaneous tension and myoplasmic free Ca21 were impaired in LCx versus LAD arteries isolated from sedentary but not exercise-trained pigs. In contrast, relaxation in response to the cAMP-dependent vasodilator forskolin (1029 to 1025 M) and the cGMP-dependent vasodilator sodium nitroprusside (1029 to 1024 M) was not different in LCx versus LAD arteries of sedentary or exercise-trained animals. These data suggest that chronic occlusion impairs receptor-dependent, cAMP-mediated relaxation; receptorindependent cAMPand cGMP-mediated relaxation were unimpaired. Importantly, exercise training restores cAMPmediated relaxation of collateral-dependent coronary arteries.