ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2015
Role played by NaV 1.7 channels on thin-fiber muscle afferents in transmitting the exercise pressor reflex.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- The Role of Ion-Transporting Proteins on Crosstalk Between the Skeletal Muscle and Central Nervous Systems Elicited by Physical Exercise.Molecular neurobiology · 2025Review
- Role of NaThe Journal of physiology · 2024Article
- Enhancement by TNF-α of TTX-resistant NaAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Looking Back on Seven Years ofAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Effects of Lactate on One Class of Group III (CT3) Muscle Afferents.Frontiers in cellular neuroscience · 2020Article
- Exaggerated exercise pressor reflex in type 2 diabetes: Potential role of oxidative stress.Autonomic neuroscience : basic & clinical · 2019Review
- Pharmacological characterization of crotamine effects on mice hind limb paralysis employing both ex vivo and in vivo assays: Insights into the involvement of voltage-gated ion channels in the crotamine action on skeletal muscles.PLoS neglected tropical diseases · 2018Article
- The mechano-gated channel inhibitor GsMTx4 reduces the exercise pressor reflex in rats with ligated femoral arteries.American journal of physiology. Heart and circulatory physiology · 2016Article
- The mechano-gated channel inhibitor GsMTx4 reduces the exercise pressor reflex in decerebrate rats.The Journal of physiology · 2016Article
- EXPRESS: Voltage-dependent sodium (NaV) channels in group IV sensory afferents.Molecular pain · 2016Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Voltage-gated sodium channels (NaV) 1.7 are highly expressed on the axons of somatic afferent neurons and are thought to play an important role in the signaling of inflammatory pain. NaV 1.7 channels are classified as tetrodotoxin (TTX)-sensitive, meaning that they are blocked by TTX concentrations of less than 300 nM. These findings prompted us to determine in decerebrated, unanesthetized rats, the role played by NaV 1.7 channels in the transmission of muscle afferent input evoking the exercise pressor reflex. We first showed that the exercise pressor reflex, which was evoked by static contraction of the triceps surae muscles, was reversibly attenuated by application of 50 nM TTX, but not 5 nM TTX, to the L4-L5 dorsal roots (control: 21 ± 1 mmHg, TTX: 8 ± 2 mmHg, recovery: 21 ± 3 mmHg; n = 6; P < 0.01). We next found that the peak pressor responses to contraction were significantly attenuated by dorsal root application of 100 nM Ssm6a, a compound that is a selective NaV 1.7 channel inhibitor. Removal of Ssm6a restored the reflex to its control level (control: 19 ± 3 mmHg, Ssm6a: 10 ± 1 mmHg, recovery: 19 ± 4 mmHg; n = 6; P < 0.05). Compound action potentials recorded from the L4 and L5 dorsal roots and evoked by single-pulse stimulation of the sciatic nerve showed that both TTX and Ssm6a attenuated input from group III, as well as group IV afferents. We conclude that NaV 1.7 channels play a role in the thin-fiber muscle afferent pathway evoking the exercise pressor reflex.
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