Balloon catheter injury abolishes phenylephrine-induced relaxation in the rat contralateral carotid

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 (Emax= 0.01 ± 0.004 g) in relation to control (Emax= 0.18 ± 0.005 g). Phenylephrine-induced contractions were increased in contralateral arteries (Emax= 0.54 ± 0.009 g) in relation to control (Emax= 0.38 ± 0.014 g). SC236 restored phenylephrine-induced relaxation (Emax= 0.17 ± 0.004 g) and contraction (Emax= 0.34 ± 0.018 g) in contralateral arteries. Tempol restored phenylephrine-induced relaxation (Emax= 0.19 ± 0.012 g) and contraction (Emax= 0.42 ± 0.014 g) in contralateral arteries, while apocynin did not alter either relaxation (Emax= 0.01 ± 0.004 g) or contraction (Emax= 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 O2- derived from COX-2.