In decerebrate rats, we reported previously that the exercise pressor reflex arising from a limb whose femoral artery was occluded for 72 h before the experiment was significantly higher than the exercise pressor reflex arising from a contralateral freely perfused limb. These findings prompted us to examine whether reactive oxygen species contributed to the augmented pressor reflex in rats with femoral artery occlusion. We found that the pressor reflex arising from the limb whose femoral artery was occluded for 72 h before the experiment (31 ± 5 mmHg) was attenuated by tempol (10 mg), a superoxide dismutase (SOD) mimetic (18 ± 5 mmHg, n = 9, P < 0.05), that was injected into the arterial supply of the hindlimb. In contrast, the pressor reflex arising from a freely perfused hindlimb (20 ± 3 mmHg) was not attenuated by tempol (17 ± 4 mmHg, n = 10, P = 0.49). Nevertheless, we found no difference in the increase in 8-isoprostaglandin F2α levels, an index of reactive oxygen species, in response to contraction between freely perfused (3.76 ± 0.82 pg/ml, n = 19) and 72-h occluded (3.51 ± 0.92 pg/ml, n = 22, P = 0.90) hindlimbs. Moreover, tempol did not reduce the 8-isoprostaglandin F2α levels during contraction in either group ( P > 0.30). A second SOD mimetic, tiron (200 mg/kg), had no effect on the exercise pressor reflex in either the rats with freely perfused hindlimbs or in those with occluded femoral arteries. These findings suggest that tempol attenuated the exercise pressor reflex in the femoral artery-occluded hindlimb by a mechanism that was independent of its ability to scavenge reactive oxygen species.
Activation of peripheral mu‐opioid receptor attenuates the augmented exercise pressor reflex seen in rats with chronic femoral artery occlusion
