Role of TNF-α in Regulating the Exercise Pressor Reflex in Rats With Femoral Artery Occlusion

Responses of sympathetic nerve activity and arterial blood pressure are augmented during activation of the exercise pressor reflex in rats with femoral artery occlusion. The present study examined the role played by proinflammatory tumor necrosis factor-α (TNF-α) in regulating augmented sympathetic...

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Main Authors: Jihong Xing, Jian Lu, Jianhua Li
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-10-01
Series:Frontiers in Physiology
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fphys.2018.01461/full
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author Jihong Xing
Jihong Xing
Jian Lu
Jianhua Li
author_facet Jihong Xing
Jihong Xing
Jian Lu
Jianhua Li
author_sort Jihong Xing
collection DOAJ
description Responses of sympathetic nerve activity and arterial blood pressure are augmented during activation of the exercise pressor reflex in rats with femoral artery occlusion. The present study examined the role played by proinflammatory tumor necrosis factor-α (TNF-α) in regulating augmented sympathetic responsiveness induced by stimulation of muscle metabolic receptors and static muscle contraction following 72 h of femoral artery occlusion. We first observed that the levels of TNF-α and protein expression of TNF-α receptor type 1 (TNFR1) were increased in the dorsal root ganglion (DRG) of hindlimbs with femoral artery occlusion. Note that TNF-α was observed within DRG neurons of C-fiber afferent nerves. Capsaicin (TRPV1 agonist) and AITC (TRPA1 agonist) were injected into arterial blood supply of the hindlimbs to stimulate metabolically sensitive thin-fiber muscle afferents. The effects of these injections on the sympathetic and pressor responses were further examined in control rats and rats with femoral artery occlusion. As TNF-α synthesis suppressor pentoxifylline (PTX) was previously administered into the hindlimb with femoral artery occlusion, sympathetic, and pressor responses induced by capsaicin and AITC were attenuated. In occluded rats, PTX also attenuated the exaggeration of blood pressure response induced by muscle contraction, but not by passive tendon stretch. Overall, the results suggest that TNF-α plays a role in modulating exaggerated sympathetic nervous activity via the metabolic component of the exercise pressor reflex when the hindlimb muscles are ischemic in peripheral arterial disease.
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spelling doaj.art-a7c958b0e2824a21a934f76a3405b19d2022-12-22T01:16:05ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2018-10-01910.3389/fphys.2018.01461417460Role of TNF-α in Regulating the Exercise Pressor Reflex in Rats With Femoral Artery OcclusionJihong Xing0Jihong Xing1Jian Lu2Jianhua Li3Heart & Vascular Institute, The Pennsylvania State University College of Medicine, Hershey, PA, United StatesDepartment of Emergency Medicine, The First Hospital of Jilin University, Changchun, ChinaHeart & Vascular Institute, The Pennsylvania State University College of Medicine, Hershey, PA, United StatesHeart & Vascular Institute, The Pennsylvania State University College of Medicine, Hershey, PA, United StatesResponses of sympathetic nerve activity and arterial blood pressure are augmented during activation of the exercise pressor reflex in rats with femoral artery occlusion. The present study examined the role played by proinflammatory tumor necrosis factor-α (TNF-α) in regulating augmented sympathetic responsiveness induced by stimulation of muscle metabolic receptors and static muscle contraction following 72 h of femoral artery occlusion. We first observed that the levels of TNF-α and protein expression of TNF-α receptor type 1 (TNFR1) were increased in the dorsal root ganglion (DRG) of hindlimbs with femoral artery occlusion. Note that TNF-α was observed within DRG neurons of C-fiber afferent nerves. Capsaicin (TRPV1 agonist) and AITC (TRPA1 agonist) were injected into arterial blood supply of the hindlimbs to stimulate metabolically sensitive thin-fiber muscle afferents. The effects of these injections on the sympathetic and pressor responses were further examined in control rats and rats with femoral artery occlusion. As TNF-α synthesis suppressor pentoxifylline (PTX) was previously administered into the hindlimb with femoral artery occlusion, sympathetic, and pressor responses induced by capsaicin and AITC were attenuated. In occluded rats, PTX also attenuated the exaggeration of blood pressure response induced by muscle contraction, but not by passive tendon stretch. Overall, the results suggest that TNF-α plays a role in modulating exaggerated sympathetic nervous activity via the metabolic component of the exercise pressor reflex when the hindlimb muscles are ischemic in peripheral arterial disease.https://www.frontiersin.org/article/10.3389/fphys.2018.01461/fullmuscle afferent nerveTNF-αperipheral arterial diseasehindlimb ischemiaexerciseblood pressure
spellingShingle Jihong Xing
Jihong Xing
Jian Lu
Jianhua Li
Role of TNF-α in Regulating the Exercise Pressor Reflex in Rats With Femoral Artery Occlusion
Frontiers in Physiology
muscle afferent nerve
TNF-α
peripheral arterial disease
hindlimb ischemia
exercise
blood pressure
title Role of TNF-α in Regulating the Exercise Pressor Reflex in Rats With Femoral Artery Occlusion
title_full Role of TNF-α in Regulating the Exercise Pressor Reflex in Rats With Femoral Artery Occlusion
title_fullStr Role of TNF-α in Regulating the Exercise Pressor Reflex in Rats With Femoral Artery Occlusion
title_full_unstemmed Role of TNF-α in Regulating the Exercise Pressor Reflex in Rats With Femoral Artery Occlusion
title_short Role of TNF-α in Regulating the Exercise Pressor Reflex in Rats With Femoral Artery Occlusion
title_sort role of tnf α in regulating the exercise pressor reflex in rats with femoral artery occlusion
topic muscle afferent nerve
TNF-α
peripheral arterial disease
hindlimb ischemia
exercise
blood pressure
url https://www.frontiersin.org/article/10.3389/fphys.2018.01461/full
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