Premium
The role of TNF‐α in femoral artery occlusion‐augmented autonomic responsiveness (1132.6)
Author(s) -
Lu Jian,
Xing Jihong,
Li Jianhua
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1132.6
Subject(s) - medicine , hindlimb , femoral artery , trpv1 , receptor , blood pressure , stimulation , endocrinology , dorsal root ganglion , sympathetic nervous system , cardiology , anatomy , anesthesia , dorsum , transient receptor potential channel
Prior studies demonstrated that metabolically sensitive receptors in thin‐fiber muscle afferents contribute to the amplified responses of sympathetic nerve activity and arterial blood pressure observed in rats with femoral artery occlusion (24‐72 hrs). The purpose of this study was to examine the role played by TNF‐α in augmented sympathetic responsiveness induced by stimulation of muscle metabolic receptors following 72 hrs of femoral artery occlusion. First, the results of this study show that the levels of TNF‐α are increased in dorsal root ganglion (DRG) neurons of limbs with 72 hrs of femoral artery occlusion. Second, protein expression of TNF‐α is dominantly observed within DRG neuron supply C‐fiber muscle afferent nerves and TNF‐α receptor type 1 (TNFR1) is largely identified in DRG compared with TNFR2. Third, TNF‐α synthesis suppressor pentoxifylline (PTX) administered previously into the hindlimb muscles significantly attenuates sympathetic and blood pressure responses induced by arterial injection of capsaicin into the hindlimb muscles. Capsaicin was applied to stimulate metabolically sensitive receptors in thin‐fiber muscle afferents nerves. Overall, our data suggest that TNF‐α plays a role in modulating augmented sympathetic responsiveness via metabolic receptors of thin fiber muscle afferent nerves when arterial blood supply to the hindlimb is deficient under ischemic conditions. Grant Funding Source : NIH P01 HL096570 and AHA EIA 0840130N