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首页> 外文期刊>American Journal of Physiology >Activation of TRPV1 in nucleus tractus solitarius reduces brown adipose tissue thermogenesis, arterial pressure, and heart rate
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Activation of TRPV1 in nucleus tractus solitarius reduces brown adipose tissue thermogenesis, arterial pressure, and heart rate

机译：核泌尿病中TRPV1的激活减少了棕色脂肪组织热生成，动脉压和心率

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摘要

The sympathetic nerve activity (SNA) to brown adipose tissue (BAT) regulates BAT thermogenesis to defend body temperature in cold environments or to produce fever during immune responses. The vagus nerve contains afferents that inhibit the BAT SNA and BAT thermogenesis evoked by skin cooling. We sought to determine whether activation of transient receptor potential vanilloid 1 (TRPV1) channels in the nucleus tractus solitarius (NTS), which are prominently expressed in unmyelinated vagal afferents, would affect cold-evoked BAT thermogenesis, cardiovascular parameters, or their vagal afferent-evoked responses. In urethane-chloralose-anesthetized rats, during skin cooling, nanoinjection of the TRPV1-agonist resiniferatoxin in NTS decreased BAT SNA (from 695 ± 195% of baseline during cooling to 103 ± 8% of baseline after resiniferatoxin), BAT temperature (?0.8 ± 0.1°C), expired CO2 (?0.3 ± 0.04%), mean arterial pressure (MAP; ?20 ± 5 mmHg), and heart rate (?44 ± 11 beats/min). Pretreatment of NTS with the TRPV1 antagonist capsazepine prevented these resiniferatoxin-mediated effects. Intravenous injection of the TRPV1 agonist dihydrocapsaicin also decreased all the measured variables (except MAP). Bilateral cervical or subdiaphragmatic vagotomy attenuated the decreases in BAT SNA and thermogenesis evoked by nanoinjection of resiniferatoxin in NTS but did not prevent the decreases in BAT SNA and BAT thermogenesis evoked by intravenous dihydrocapsaicin. We conclude that activation of TRPV1 channels in the NTS of vagus nerve intact rats inhibits BAT SNA and decreases BAT metabolism, blood pressure, and heart rate. In contrast, the inhibition of BAT thermogenesis following systemic administration of dihydrocapsaicin does not require vagal afferent activity, consistent with a nonvagal pathway through which systemic TRPV1 agonists can inhibit BAT thermogenesis.
机译：棕色脂肪组织（蝙蝠）的交感神经活动（SNA）调节蝙蝠热量，以防止冷环境中的体温或在免疫反应期间产生发热。迷走神经含有抑制皮肤冷却引起的蝙蝠SNA和蝙蝠热量的传统。我们试图确定在未封闭的缩小发动中突出地表达的鼻窦菌毒素（NTS）中的瞬态受体潜在的潜在香毒素1（TRPV1）通道的激活会影响冷诱发的蝙蝠热生成，心血管参数，或迷失 - 诱发的反应。在氨基甲酸氢卤代丙酮溶血化大鼠中，在皮肤冷却过程中，NTS中的TRPV1激动剂树脂植物毒素的纳米注射减少了蝙蝠SNA（从冷却至103±8％的基线中，在树脂植物毒素后的103±8％），蝙蝠温度（？0.8 ±0.1°C），过期二氧化碳（α0.3±0.04％），平均动脉压（MAP; 2±5mmHg）和心率（？44±11次/分钟）。用TRPV1拮抗剂胶囊化动物预处理NTS预防这些树脂肽毒素介导的效果。静脉注射TRPV1激动剂二氢磷藻蛋白也降低了所有测量的变量（除图谱）。双侧宫颈或副椎间膜透露术减弱蝙蝠SNA的降低，并通过NTS的树脂素毒素纳米注射诱导的热生成，但并未阻止通过静脉注射二氢磷藻蛋白引发的蝙蝠SNA和蝙蝠热量降低。我们得出结论，迷走神经完整大鼠NTS中TRPV1通道的激活抑制了蝙蝠SNA，降低了蝙蝠代谢，血压和心率。相反，在系统施用二氢磷蛋白的全身施用后对蝙蝠热生成的抑制不需要缩小的传入活性，与天系统的TRPV1激动剂可以抑制蝙蝠热量的非游戏途径一致。

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