title: Effects of N-nitro-L-arginine on coronary artery tone and reactive hyperemia after brief coronary occlusion in conscious dogs.
abstract: OBJECTIVE
  To determine the role of an endothelium-derived relaxing factor (nitric oxide) in controlling basal coronary tone and coronary vasomotion after brief coronary occlusion (reactive hyperemia).
  
  
  METHODS
  In 10 chronically instrumented conscious dogs, we studied the diameter changes of the large epicardial coronary artery and coronary blood flow in response to intracoronary administration of acetylcholine (0.1 and 1 microgram) and brief coronary occlusion for 5 and 20 s before and after intracoronary infusion of N-nitro-L-arginine (LNNA).
  
  
  RESULTS
  Intracoronary infusion of LNNA (1, 3, and 10 mg) decreased the diameter of the large epicardial coronary artery and coronary blood flow in a dose-dependent manner without altering arterial pressure and heart rate. LNNA (10 mg) significantly attenuated the increase in artery diameter and coronary blood flow by acetylcholine. The ratio of artery dilation to the blood flow response after acetylcholine was not affected by LNNA. LNNA (10 mg) significantly decreased the ratio of repayment to debt flow volume of reactive hyperemia, but did not affect the ratio of peak to resting flow; it also significantly attenuated the reactive dilation of the large epicardial coronary artery after reactive hyperemia. The ratio of artery dilation to repayment flow volume (micron/ml) during reactive hyperemia was attenuated significantly by LNNA.
  
  
  CONCLUSIONS
  These findings suggest that endothelium-derived nitric oxide may contribute to basal coronary tone and that reactive dilation of the large epicardial coronary artery during reactive hyperemia was caused by flow-mediated nitric oxide release, whereas coronary artery dilation after acetylcholine was caused largely by the direct receptor-mediated release of nitric oxide.
authors.affiliation: Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Muramatsu
authors.forename: K
authors.initials: K
authors.lastname: Numaguchi
authors.forename: K
authors.initials: K
authors.lastname: Egashira
authors.forename: T
authors.initials: T
authors.lastname: Takahashi
authors.forename: H
authors.initials: H
authors.lastname: Kasuya
authors.forename: A
authors.initials: A
authors.lastname: Takeshita
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology; D001783:Blood Flow Velocity / Q000187:drug effects; D003243:Consciousness; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000150:complications* / Q000378:metabolism; D003331:Coronary Vessels / Q000187:drug effects* / Q000378:metabolism; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000378:metabolism; D006940:Hyperemia / Q000209:etiology / Q000378:metabolism*; D009569:Nitric Oxide / Q000096:biosynthesis / Q000378:metabolism*; D019335:Nitroarginine; D014664:Vasodilation / Q000187:drug effects
chemical_list: D019335:Nitroarginine; D009569:Nitric Oxide; D001120:Arginine; D000109:Acetylcholine