Evidence Details for Trpv1
PMID Title Journal Year Abstract
37384285 Attenuation of immobilization stress-induced hypertension by temperature-controllable warm needle acupuncture in rats and the peripheral neural mechanisms. Front Neurol. 2023 Jun 13;14:1168012. doi: 10.3389/fneur.2023.1168012. eCollection 2023. 2023 INTRODUCTION: We and others have shown that electrical stimulation of the PC-6 acupoint over the wrist relieves hypertension by stimulating afferent sensory nerve fibers and activating the central endogenous opioid system. Warm needle acupuncture has long been utilized to treat various diseases in clinics. METHODS: Here, we developed a temperature-controllable warm needle acupuncture instrument (WAI) and investigated the peripheral mechanism underlying the effect of warm needle acupuncture at PC-6 on hypertension in a rat model of immobilization stress-induced hypertension. RESULTS: Stimulation with our newly developed WAI and traditional warm needle acupuncture attenuated hypertension development. Such effects were reproduced by capsaicin (a TRPV1 agonist) injection into PC-6 or WAI stimulation at 48 degrees C. In contrast, PC-6 pretreatment with the TRPV1 antagonist capsazepine blocked the antihypertensive effect of WAI stimulation at PC-6. WAI stimulation at PC-6 increased the number of dorsal root ganglia double-stained with TRPV1 and CGRP. QX-314 and capsaicin perineural injection into the median nerve for chemical ablation of small afferent nerve fibers (C-fibers) prevented the antihypertensive effect of WAI stimulation at PC-6. Additionally, PC-6 pretreatment with RTX ablated the antihypertensive effect of WAI stimulation. CONCLUSION: These findings suggest that warm needle acupuncture at PC-6 activates C-fiber of median nerve and the peripheral TRPV1 receptors to attenuate the development of immobilization stress-induced hypertension in rats."

Evidence Sentence: WAI stimulation at PC-6 increased the number of dorsal root ganglia double-stained with TRPV1 and CGRP.
Evidence Sentence: To explore which subtypes of TRPV1-expressing DRG neurons were activated by WAI stimulation at PC-6, double-staining of TRPV1 and the neuronal markers CGRP (a peptidergic small neuronal marker), IB4 (a nonpeptidergic small neuronal marker) or NF200 (a marker for sensory myelinated fibers) was performed.
Evidence Sentence: The fluorescence intensity of TRPV1-immunoreactive neurons colocalized with CGRP was significantly higher in the WAI-stimulated group (n = 6) than in the normal group (Figures 5A,B) (t-test, F = 3.164, p < 0.001), and the number of TRPV1 neurons double-labeled with IB4 was significantly higher in the WAI group (n = 6) than in the normal group (Figures 5E,F) (n = 6, t-test, F = 1.249, p < 0.05).
Evidence Sentence: On the other hand, few neurons were double-labeled with NF200 and TRPV1 in the either the normal group or the WAI group (Figures 5C,D).
Evidence Sentence: Inhibition of the PC-6-stimulation antihypertensive effect by ablating TRPV1 with RTX
Evidence Sentence: To observe the activation of TRPV1 by WAI stimulation at 48 C, immunohistochemistry for TRPV1 in the DRGs of C6-T2 was carried out in another set of animals.
Evidence Sentence: An almost 2-fold increase in TRPV1 was found in the WAI group compared with the normal group (t-test, F = 4.806, p < 0.0001; Figures 4C,D).
Evidence Sentence: To identify whether the ablation of peripheral TRPV1 channels at PC-6 inhibited the antihypertensive effect of WAI stimulation at PC-6, RTX, known to desensitize TRPV1 receptors, was injected into PC-6 in rats with IMH.
Evidence Sentence: Immunohistochemistry for TRPV1 showed that the enhanced expression of TRPV1 induced by WAI stimulation at PC-6 was suppressed by pretreatment with RTX prior to WAI stimulation (one-way ANOVA; F=13.22, p < 0.0001; Figures 6B,C).
Evidence Sentence: To explore whether the antihypertensive effect of WAI stimulation at PC-6 is mediated through peripheral TRPV1 receptors, the TRPV1 antagonist capsazepine was injected into the PC-6 acupoint 40 min prior to the experiment.
Evidence Sentence: To further confirm whether the activation of TRPV1 receptors at PC-6 itself can produce antihypertensive effects, the TRPV1 agonist capsaicin was injected into PC-6 10 min prior to immobilization stress.
Evidence Sentence: Such effects were reproduced by capsaicin (a TRPV1 agonist) injection into PC-6 or WAI stimulation at 48 C. In contrast, PC-6 pretreatment with the TRPV1 antagonist capsazepine blocked the antihypertensive effect of WAI stimulation at PC-6.