dc.creator | PERNOMIAN, L. | |
dc.creator | GOMES, M. S. | |
dc.creator | OLIVEIRA, A. M. de | |
dc.date.accessioned | 2012-10-19T03:40:07Z | |
dc.date.accessioned | 2018-07-04T14:57:17Z | |
dc.date.available | 2012-10-19T03:40:07Z | |
dc.date.available | 2018-07-04T14:57:17Z | |
dc.date.created | 2012-10-19T03:40:07Z | |
dc.date.issued | 2011 | |
dc.identifier | BRITISH JOURNAL OF PHARMACOLOGY, v.163, n.4, p.770-781, 2011 | |
dc.identifier | 0007-1188 | |
dc.identifier | http://producao.usp.br/handle/BDPI/19962 | |
dc.identifier | 10.1111/j.1476-5381.2011.01275.x | |
dc.identifier | http://dx.doi.org/10.1111/j.1476-5381.2011.01275.x | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1616746 | |
dc.description.abstract | BACKGROUND AND PURPOSE 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. EXPERIMENTAL APPROACH 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. KEY 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 AND IMPLICATIONS Balloon catheter injury abolished phenylephrine-induced relaxation and increased phenylephrine-induced contraction in contralateral carotid arteries, through O(2)(-) derived from COX-2. | |
dc.language | eng | |
dc.publisher | WILEY-BLACKWELL | |
dc.relation | British Journal of Pharmacology | |
dc.rights | Copyright WILEY-BLACKWELL | |
dc.rights | restrictedAccess | |
dc.subject | balloon catheter injury | |
dc.subject | contralateral carotid artery | |
dc.subject | phenylephrine-induced relaxation | |
dc.subject | cyclooxygenase 2 | |
dc.subject | superoxide | |
dc.title | Balloon catheter injury abolishes phenylephrine-induced relaxation in the rat contralateral carotid | |
dc.type | Artículos de revistas | |