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

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.

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.

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).

Balloon catheter injury abolished phenylephrine-induced relaxation and increased phenylephrine-induced contraction in contralateral carotid arteries, through O(2) (-) derived from COX-2.