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延髓头端腹外侧部阿片受体亚型在电针抑制猫反射性自主反应中的作用

Rostral ventrolateral medullary opioid receptor subtypes in the inhibitory effect of electroacupuncture on reflex autonomic response in cats.

作者信息

Li P, Tjen-A-Looi S, Longhurst J C

机构信息

Department of Medicine, College of Medicine, University of California, Irvine 92697-4075, USA.

出版信息

Auton Neurosci. 2001 Jun 20;89(1-2):38-47. doi: 10.1016/S1566-0702(01)00247-8.

Abstract

Electroacupuncture (EA) is used in traditional Chinese medicine to treat arrhythmias, hypertension and myocardial ischemia. Our previous work suggests that the inhibitory effect of EA on the pressor reflex induced by bradykinin (BK) applied to the gallbladder is due, in part, to the activation of opioid receptors, most likely located in the rostral ventrolateral medulla (rVLM). However, specific opioid receptor subtypes, and hence the neurotransmitters. responsible for this inhibition are unknown. Therefore, in anesthetized cats, BK (10 microg/ml) was applied to the gallbladder to induce transient reflex increases in arterial blood pressure (BP). EA (1-2 mA, 5 Hz, 0.5 ms pulses) was delivered through acupuncture needles inserted bilaterally into Neiguan and Jianshi acupoints on forelimbs, overlying the median nerves. EA attenuated the BK-induced pressor response by 39%. Opioid receptor subtype antagonists or agonists were microinjected unilaterally into the rVLM. The mu- and delta-receptor antagonists CTOP and ICI 174,864, respectively, significantly attenuated the EA-induced inhibition for at least 30 min. The K-receptor antagonist (nor-BNI) was less effective and was shorter acting. Like EA, microinjection of mu- and delta-opioid agonists, DAGO and DADLE, respectively, into the rVLM significantly decreased the pressor responses. In contrast, the kappa-opioid agonist, U50,488, failed to alter the BK-induced pressor response. We conclude that a significant portion of inhibition of the gallbladder pressor response by EA is related to activation of mu- and delta-opioid receptors in the rVLM. The endogenous neurotransmitters for mu- and delta-opioid receptors, beta-endorphins and enkephalins, in the rVLM, therefore appear to play a role in the EA-related modulation of cardiovascular reflex responses. Conversely, dynorphin is less likely to be involved in this response.

摘要

电针在中医中用于治疗心律失常、高血压和心肌缺血。我们之前的研究表明,电针对胆囊应用缓激肽(BK)诱导的升压反射的抑制作用,部分归因于阿片受体的激活,这些受体很可能位于延髓头端腹外侧区(rVLM)。然而,具体的阿片受体亚型以及负责这种抑制作用的神经递质尚不清楚。因此,在麻醉猫中,将BK(10微克/毫升)应用于胆囊以诱导动脉血压(BP)的短暂反射性升高。通过双侧插入前肢内关和间使穴位(位于正中神经上方)的针灸针施加电针(1 - 2毫安,5赫兹,0.5毫秒脉冲)。电针使BK诱导的升压反应减弱了39%。将阿片受体亚型拮抗剂或激动剂单侧微量注射到rVLM中。μ-和δ-受体拮抗剂CTOP和ICI 174,864分别显著减弱了电针诱导的抑制作用,至少持续30分钟。κ-受体拮抗剂(nor-BNI)效果较差且作用时间较短。与电针类似,分别将μ-和δ-阿片激动剂DAGO和DADLE微量注射到rVLM中,显著降低了升压反应。相比之下,κ-阿片激动剂U50,488未能改变BK诱导的升压反应。我们得出结论,电针抑制胆囊升压反应的很大一部分与rVLM中μ-和δ-阿片受体的激活有关。因此,rVLM中μ-和δ-阿片受体的内源性神经递质β-内啡肽和脑啡肽似乎在电针相关的心血管反射反应调节中发挥作用。相反,强啡肽不太可能参与此反应。

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