Chronic femoral artery occlusion augments exercise pressor reflex in decerebrated rats

Abstract

In decerebrated rats, we determined the pressor and cardioaccelerator reflex responses to static contraction of hindlimb muscles whose femoral arteries were either occluded 72 h before contraction, occluded 3 min before contraction, or freely perfused. We found that the pressor reflex arising from the limb whose femoral artery was occluded for 72 h before contraction (32 +/- 5 mmHg, n = 16) was significantly higher than the pressor reflex arising from the contralateral freely perfused limb (15 +/- 3 mmHg, n = 16, P < 0.001) or than that arising from the contralateral limb whose femoral artery was occluded for only 3 min (17 +/- 4 mmHg, n = 16, P < 0.001). Moreover, the pressor reflex arising from the limb whose femoral artery was occluded for 3 min before the start of contraction was not significantly different than that arising from the contralateral freely perfused limb (n = 16, P = 0.819). The pressor component of the reflex arising from the limb whose femoral artery was occluded for 72 h was not changed by transient receptor potential vanilloid (TRPV) 1 receptor blockade with iodo-resiniferatoxin (n = 15, P = 0.272), although the cardioaccelerator component was significantly reduced (P = 0.005). In addition, the pressor response evoked by capsaicin injection in the femoral artery of the 72-h occluded limb was more than double that evoked from the freely perfused limb (P = 0.026). We conclude that chronic (i.e., 72 h) but not acute (3 min), femoral arterial occlusion augments pressor reflex arising from contraction of hindlimb muscles and that TRPV1 receptors play little role in this augmentation.

Fig. 1.

Time courses of the average changes in mean arterial pressure (MAP), heart rate (HR), and the triceps surae muscle tension during static contraction: 72-h occluded vs. freely perfused limb. The overall pressor response to static contraction was larger in the 72-h occluded limb than in the freely perfused limb. The time course of the changes in HR was similar irrespective of the limb conditions. Values belonging to the same treatments of the femoral artery were pooled. Values are means ± SE (n = 16 rats) and plotted at 1-s intervals.

Fig. 2.

Time courses of the average changes in MAP, HR, and the triceps surae muscle tension during static contraction: 72-h occluded vs. 3-min occluded limb. The overall pressor response to static contraction was larger in the 72-h occluded limb than in the 3-min occluded limb. The time course of the changes in HR was similar irrespective of the limb conditions. Values belonging to the same treatments of the femoral artery were pooled. Values are means ± SE (n = 16) and plotted at 1-s intervals.

Fig. 3.

Time courses of the average changes in MAP, HR, and the triceps surae muscle tension during static contraction: 3-min occluded vs. freely perfused limb. The overall pressor and cardioaccelerator responses to static contraction were similar irrespective of the limb conditions. Values belonging to the same treatments of the femoral artery were pooled. Values are means ± SE (n = 16) and plotted at 1-s intervals.

Fig. 4.

Peak increases in MAP and HR during static contraction. The peak increases of MAP during static contraction in 72-h occluded limb were almost two times as large as that in freely perfused or 3-min occluded limb. Three minutes of acute femoral artery occlusion did not augment the pressor response compared with freely perfused limb during static contraction. The differences of the peak increases in HR during static contraction were not statistically significant among these limbs. Values are means ± SE (n = 16). The pressor responses to contraction in each of the three conditions were significantly increased from their respective baselines (*P < 0.05). Horizontal brackets signify that the increases are significantly different from each other (†P < 0.05).

Fig. 5.

Effects of administration of iodo-resiniferatoxin (IRTX) from two different routes on peak MAP and HR responses during static contraction. IRTX was administered either retrogradely in contralateral (A, n = 10) or anterogradely in ipsilateral (B, n = 5) femoral artery. Values under the x-axis labels are their baseline values. The pressor and HR responses to contraction in each condition were significantly increased from their respective baselines (*P < 0.05). A: retrograde administration of IRTX did not affect the peak increases of MAP but decreased the peak HR responses during static contraction in 72-h occluded limb. B: anterograde administration of IRTX did not affect either peak MAP or HR responses to static contraction. Values are means ± SE.

Fig. 6.

Effects of IRTX on peak MAP and HR responses during static contraction (A) and during intra-arterial injection of capsaicin (B). The data from the 15 rats injected with IRTX were combined. Values under the x-axis labels are their baseline values. A: the peak MAP and HR values during static contraction were significantly increased from their respective baselines (*P < 0.05). IRTX (10 μg) had no significant effect on the peak pressor response to static contraction (P = 0.272), whereas the antagonist significantly decreased the peak cardioaccelerator responses to contraction (P = 0.007). B: the peak MAP and HR responses to capsaicin injection in femoral circulation were significantly attenuated by pretreatment of IRTX. Horizontal brackets signify that the increases are significantly different from each other (†P < 0.05). Values are means ± SE (n = 15).

Fig. 7.

Effects of capsaicin (0.5 μg) injected in the femoral artery on MAP and HR. Nos. under the x-axis are baseline values. *Significant increase in either MAP or HR over its respective baseline value. Horizontal bracket represents significant difference between pressor response to capsaicin in rats whose femoral artery was freely perfused and rats whose femoral artery was occluded for 72 h.