title: Balloon catheter injury abolishes phenylephrine-induced relaxation in the rat contralateral carotid.
abstract: OBJECTIVE
  The consequences of compensatory responses to balloon catheter injury in rat carotid artery, on phenylephrine-induced relaxation and contraction in the contralateral carotid artery were studied.
  
  
  METHODS
  Relaxation and contraction concentration-response curves for phenylephrine were obtained for contralateral carotid arteries in the presence of indomethacin (COX inhibitor), SC560 (COX-1 inhibitor), SC236 (COX-2 inhibitor) or 4-hydroxytetramethyl-L-piperidine-1-oxyl (tempol; superoxide dismutase mimetic). Reactive oxygen species were measured in carotid artery endothelial cells fluorimetrically with dihydroethidium.
  
  
  RESULTS
  Phenylephrine-induced relaxation was abolished in contralateral carotid arteries from operated rats (E(max) = 0.01 ± 0.004 g) in relation to control (E(max) = 0.18 ± 0.005 g). Phenylephrine-induced contractions were increased in contralateral arteries (E(max) = 0.54 ± 0.009 g) in relation to control (E(max) = 0.38 ± 0.014 g). SC236 restored phenylephrine-induced relaxation (E(max) = 0.17 ± 0.004 g) and contraction (E(max) = 0.34 ± 0.018 g) in contralateral arteries. Tempol restored phenylephrine-induced relaxation (E(max) = 0.19 ± 0.012 g) and contraction (E(max) = 0.42 ± 0.014 g) in contralateral arteries, while apocynin did not alter either relaxation (E(max) = 0.01 ± 0.004 g) or contraction (E(max) = 0.54 ± 0.009 g). Dihydroethidium fluorescence was increased in contralateral samples (18 882 ± 435 U) in relation to control (10 455 ± 303 U). SC236 reduced the fluorescence in contralateral samples (8250 ± 365 U).
  
  
  CONCLUSIONS
  Balloon catheter injury abolished phenylephrine-induced relaxation and increased phenylephrine-induced contraction in contralateral carotid arteries, through O(2) (-) derived from COX-2.
authors.affiliation: Department of Pharmacology, School of Medicine of Ribeirão Preto, Laboratory of Pharmacology, University of São Paulo, Brazil.
authors.forename: L
authors.initials: L
authors.lastname: Pernomian
authors.forename: Ms
authors.initials: M
authors.lastname: Gomes
authors.forename: Am
authors.initials: A
authors.lastname: de Oliveira
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000818:Animals; D002339:Carotid Arteries / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D020212:Carotid Artery Injuries / Q000378:metabolism / Q000503:physiopathology*; D003497:Cyclic N-Oxides / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000293:injuries; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism; D009249:NADP / Q000378:metabolism; D019255:NADPH Oxidases / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D010656:Phenylephrine / Q000494:pharmacology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D011720:Pyrazoles / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013113:Spin Labels; D013449:Sulfonamides / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects*; D000096926:Benzenesulfonamides
chemical_list: D003497:Cyclic N-Oxides; D016861:Cyclooxygenase Inhibitors; D007213:Indomethacin; D009249:NADP; D019255:NADPH Oxidases; D010100:Oxygen; D010656:Phenylephrine; D011451:Prostaglandin-Endoperoxide Synthases; D011720:Pyrazoles; D017382:Reactive Oxygen Species; D013113:Spin Labels; D013449:Sulfonamides; C119130:4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide; D000096926:Benzenesulfonamides; C115461:SC 560; C001803:tempol