title: Exercise training restores adenosine-induced relaxation in coronary arteries distal to chronic occlusion.
abstract: 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 cAMP- versus 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 (10(-7) to 10(-3) M) and isoproterenol (3 x 10(-8) to 3 x 10(-5) 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 Ca(2+) 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 (10(-9) to 10(-5) M) and the cGMP-dependent vasodilator sodium nitroprusside (10(-9) to 10(-4) 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; receptor-independent cAMP- and cGMP-mediated relaxation were unimpaired. Importantly, exercise training restores cAMP-mediated relaxation of collateral-dependent coronary arteries.
authors.affiliation: Dalton Cardiovascular Research Center, University of Missouri, Columbia 65211, USA.
authors.forename: C L
authors.initials: CL
authors.lastname: Heaps
authors.forename: M
authors.initials: M
authors.lastname: Sturek
authors.forename: J A
authors.initials: JA
authors.lastname: Rapps
authors.forename: M H
authors.initials: MH
authors.lastname: Laughlin
authors.forename: J L
authors.initials: JL
authors.lastname: Parker
mesh_terms: D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D002908:Chronic Disease; D005576:Colforsin / Q000494:pharmacology; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects* / Q000503:physiopathology*; D005260:Female; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D009994:Osmolar Concentration; D010805:Physical Conditioning, Animal; D013552:Swine; D013556:Swine, Miniature; D014664:Vasodilation / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D005576:Colforsin; D000241:Adenosine; D007545:Isoproterenol; D002118:Calcium