title: Exercise training improves endothelium-mediated vasorelaxation after chronic coronary occlusion.
abstract: 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 microm 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 N(G)-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.
authors.affiliation: Dalton Cardiovascular Research Center, University of Missouri, Columbia 65211, USA.
authors.forename: K L
authors.initials: KL
authors.lastname: Griffin
authors.forename: M H
authors.initials: MH
authors.lastname: Laughlin
authors.forename: J L
authors.initials: JL
authors.lastname: Parker
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D001685:Biological Factors / Q000096:biosynthesis; D001920:Bradykinin / Q000494:pharmacology; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D003331:Coronary Vessels / Q000502:physiology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D009200:Myocardial Contraction / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000235:genetics; D052250:Nitric Oxide Synthase Type III; D010084:Oxidation-Reduction; D010805:Physical Conditioning, Animal / Q000502:physiology*; D013552:Swine; D013556:Swine, Miniature; D014664:Vasodilation / Q000502:physiology*
chemical_list: D001685:Biological Factors; D004791:Enzyme Inhibitors; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide; D000244:Adenosine Diphosphate; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D001920:Bradykinin; D019331:NG-Nitroarginine Methyl Ester