Disease relevance of TRPV1

• Here, we report that TRPV1 antagonists representing various chemotypes cause an increase in body temperature (hyperthermia), identifying a potential issue for their clinical development [1].

High impact information on TRPV1

• Deletion of vanilloid receptor 1-expressing primary afferent neurons for pain control [2].
• 4. Lactic acid-evoked increases in RL were unaffected by VR1 blockade with capsazepine, consistent with a separate lactic acid-induced reflex mechanism [3].
• 1. Capsaicin activation of the pulmonary C fibre vanilloid receptor (VR1) evokes the pulmonary chemoreflex and reflex bronchoconstriction [3].
• The effects of capsazepine are consistent with reversible blockade of the VR1 receptor to abolish C fibre-mediated reflex bronchoconstriction [3].
• TRPV1 regulators mediate gentamicin penetration of cultured kidney cells [4].

Chemical compound and disease context of TRPV1

• Antagonists that are ineffective against proton activation also caused hyperthermia, indicating that blocking capsaicin and heat activation of TRPV1 is sufficient to produce hyperthermia [1].

Biological context of TRPV1

• Together, these results indicate that tonic TRPV1 activation regulates body temperature [1].
• TRPV1 antagonists caused hyperthermia in multiple species (rats, dogs, and monkeys), demonstrating that TRPV1 function in thermoregulation is conserved from rodents to primates [1].

Anatomical context of TRPV1

• Both kidney epithelial and inner ear sensory cells express TRPV1, are mechanosensors and accumulate the aminoglycoside antibiotic gentamicin [4].

Associations of TRPV1 with chemical compounds

• GTTR uptake was enhanced by the TRPV1 agonists, resiniferatoxin and anandamide, in Ca2+-free media [4].

References