Nociceptin in rVLM mediates electroacupuncture inhibition of cardiovascular reflex excitatory response in rats
Nociceptin in rVLM mediates electroacupuncture inhibition of cardiovascular reflex excitatory response in rats
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DOI：
10.1152/japplphysiol.01282.2004
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发表时间：
2005-06-01
影响因子：
3.3
通讯作者：
Longhurst, JC
中科院分区：
文献类型：
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作者：
Crisostomo, MM;Li, P;Longhurst, JC
电针内关-间室穴通过阿片机制抑制胃机械刺激引起的心血管升压反应。由于痛敏素也可以通过其在脑干中的作用来调节心血管活动，因此我们假设这种神经调质在EA相关的抑制作用中起作用。在胃气球充气期间测量了用氯胺酮和α-氯阿洛糖麻醉的通气雄性Sprague-Dawley大鼠（400 - 600 g）的血压。用6 - 8 ml空气进行胃扩张可诱导26 +/- 1 mmHg的一致性升压反射，每10 min重复一次，持续100 min。当将伤害感受素（10 nM）微量注射到延髓头端腹外侧（rVLM）时，胃扩张诱导的升压反应被抑制68 +/-6%。电针30分钟也使反射反应降低75 +/- 11%;向rVLM中微量注射生理盐水并不改变电针的抑制作用。与此相反，在rVLM中微量注射痛敏素受体拮抗剂可迅速逆转EA反应。阿片受体拮抗剂纳洛酮预处理不影响痛敏素对扩张诱导的升压反射（22 +/- 1至8 +/- 2 mmHg）的EA样抑制作用。此外，μ阿片受体激动剂微量注射到rVLM后，在EA期间微量注射痛敏素受体拮抗剂迅速逆转痛敏素受体拮抗剂相关的抑制EA效应。因此，除了经典的阿片系统，伤害感受素，通过阿片受体样受体1受体的刺激在rVLM，参与调制影响EA反射引起的血压升高。
Electroacupuncture (EA) at Neiguan-Jianshi acupoints through an opioid mechanism inhibits the cardiovascular pressor response induced by mechanical stimulation of the stomach. Because nociceptin also may regulate cardiovascular activity through its action in the brain stem, we hypothesized that this neuromodulator serves a role in the EA-related inhibitory effect. Blood pressure in ventilated male Sprague-Dawley rats ( 400 - 600 g) anesthetized by ketamine and alpha-chloralose was measured during balloon inflation of the stomach. Gastric distension with 6 - 8 ml of air induced consistent pressor reflexes of 26 +/- 1 mmHg that could be repeated every 10 min for 100 min. When nociceptin ( 10 nM) was microinjected into the rostral ventrolateral medulla (rVLM), the pressor response induced by gastric distension was inhibited by 68 +/- 6%. Thirty minutes of EA also decreased the reflex response by 75 +/- 11%; microinjection of saline into the rVLM did not alter the inhibitory effect of EA. In contrast, microinjection of a nociceptin receptor antagonist into the rVLM promptly reversed the EA response. Pretreatment with the opioid receptor antagonist naloxone did not influence the EA-like inhibitory effect of nociceptin on the distension-induced pressor reflex ( 22 +/- 1 to 8 +/- 2 mmHg). Furthermore, a mu-opioid receptor agonist microinjected into the rVLM after microinjection of a nociceptin receptor antagonist during EA promptly reversed the nociceptin receptor antagonist-related inhibition of the EA effect. Thus, in addition to the classical opioid system, nociceptin, through opioid receptor-like-1 receptor stimulation in the rVLM, participates in the modulatory influence of EA on reflex-induced increases in blood pressure.