Abstract
A rat model of femoral artery occlusion was employed to study the exercise pressor reflex in peripheral artery disease. Prior studies have shown that pro‐inflammatory interleukin‐6 (IL‐6) is engaged in the amplified blood pressure response to static muscle contraction in occluded rats. IL‐6 complexes with soluble IL‐6 receptor (IL‐6R) to activate cells expressing the signal transducer glycoprotein (gp130). Thus, the current study was to determine the role played by IL‐6 activated signal complex (IL‐6‐gp130) in regulating the exercise pressor reflex in rats with femoral occlusion. Following 72 hours of femoral artery occlusion, the levels of protein expression of IL‐6R and gp130 were increased in dorsal root ganglion (DRG). In addition, we examined the pressor response to static muscle contraction after 62.5 ng/kg and 125 ng/kg of SC144 (a gp130 inhibitor) were injected into the arterial blood supply of the hindlimb muscle of control rats and occluded rats. We found that SC144 significantly attenuated the pressor response to contraction in occluded rats, but the effect of SC144 was not observed in control rats. In control rats, peak response of mean arterial pressure (MAP) was 15±2 mmHg after saline and 12±3 mmHg after 125 ng/kg of SC144 (n=6; P > 0.05 vs. saline). In occluded rats, peak MAP response was 25±5 mmHg after saline and 14±5 mmHg after 125 ng/kg of SC144 (n=6; P < 0.05 vs. saline). There was no difference in developed muscle tension between saline group and group injected with SC144 (528±28 g in saline control vs. 545±29 g with SC144 injection, P > 0.05). Overall, our data suggest that IL‐6 signal mechanisms in muscle sensory nerves contribute to the exaggerated sympathetic and pressor responsiveness observed during exercise in experimental rats with peripheral artery disease.Support or Funding InformationThis study was supported by NIH P01 HL134609This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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