title: Intracoronary administration of adenosine triphosphate increases coronary blood flow and attenuates the severity of myocardial ischemic injury in dogs.
abstract: ATP generates nitric oxide (NO) via activation of P2y receptors, and is degraded to adenosine. This study was undertaken to examine whether ATP causes coronary hyperemic flow via purinoceptors-, NO- and adenosine-dependent mechanisms, and attenuates the severity of contractile and metabolic dysfunction in the ischemic myocardium. In the non-ischemic canine hearts, the infusions of ATP into the coronary artery dose-dependently increased coronary blood flow. The levels of adenosine and end-product of NO in coronary venous blood over the arterial blood also increased. This hyperemic flow was partially attenuated by either 8-sulfophenyltheophylline (8SPT) or L(omega)-nitro arginine methyl ester (L-NAME), and completely blocked by the treatment with 8SPT, L-NAME and suramin (SRM). During myocardial ischemia, exogenous ATP increased coronary blood flow, and attenuated myocardial metabolic and contractile dysfunction, which was completely blunted by the treatment with 8SPT, L-NAME and SRM. We conclude that exogenous ATP increases coronary blood flow in the non-ischemic and ischemic myocardium mainly via either NO- or adenosine-dependent mechanisms.
authors.affiliation: Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Japan. kitakaze@medone.med.osaka-u.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Kitakaze
authors.forename: K
authors.initials: K
authors.lastname: Node
authors.forename: K
authors.initials: K
authors.lastname: Komamura
authors.forename: T
authors.initials: T
authors.lastname: Minamino
authors.forename: H
authors.initials: H
authors.lastname: Kosaka
authors.forename: T
authors.initials: T
authors.lastname: Kuzuya
authors.forename: M
authors.initials: M
authors.lastname: Hori
mesh_terms: D000255:Adenosine Triphosphate / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D000704:Analysis of Variance; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects*; D004285:Dogs; D004791:Enzyme Inhibitors / Q000494:pharmacology; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000503:physiopathology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D011983:Receptors, Purinergic / Q000187:drug effects; D013806:Theophylline / Q000031:analogs & derivatives / Q000494:pharmacology; D014665:Vasodilator Agents / Q000097:blood
chemical_list: D004791:Enzyme Inhibitors; D011983:Receptors, Purinergic; D014665:Vasodilator Agents; D009569:Nitric Oxide; C031433:8-(4-sulfophenyl)theophylline; D000255:Adenosine Triphosphate; D013806:Theophylline; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine