What do we understand from clinical and mechanistic studies on acupuncture treatment for hypertension?
What do we understand from clinical and mechanistic studies on acupuncture treatment for hypertension?
复制标题
DOI：
10.1186/s13020-015-0070-9
复制
发表时间：
2015
期刊：
影响因子：
4.9
通讯作者：
Longhurst JC
中科院分区：
文献类型：
--
作者：
Cheng L;Li P;Tjen-A-Looi SC;Longhurst JC
针灸治疗高血压的结果尚无定论。本研究的目的是评估针灸对高血压的影响，基于几十年来的机制研究，特别是那些在加州大学欧文分校进行的研究结果。P5-6（覆盖正中神经）和S36-37（覆盖腓深神经）的低电流和低频电针（EA）以缓慢（4-8周）但持久（1-2个月）的方式降低了轻度至中度高血压患者亚组（约70%）的高血压。电针通过激活下丘脑弓状核、中脑腹外侧导水管周围灰质和延髓中缝苍白核的神经元，抑制延髓头端腹外侧区（rVLM）运动前交感神经元的活动，从而抑制心血管交感兴奋神经元的活动。多种神经递质如谷氨酸、乙酰胆碱、阿片类物质、GABA、痛敏素、5-羟色胺和内源性大麻素参与了EA诱导的兴奋反应。电针对高血压的长期抑制作用与rVLM中的阿片类物质和GABA、弓状核和腹外侧中脑导水管周围灰质之间的神经回路以及rVLM和弓状核中前脑啡肽原mRNA水平和脑啡肽水平增加的时间延长有关。此外，电针对交感神经活动的长期抑制作用在电针治疗的高血压患者中得到证实，这些患者的去甲肾上腺素、肾素和醛固酮水平降低。
The outcome of acupuncture on hypertension treatment is inconclusive. This study aims to evaluate the influence of acupuncture on hypertension, based on findings from mechanistic studies over the course of decades particularly those conducted at the University of California, Irvine. Low-current and low-frequency electroacupuncture (EA) at P5–6 (overlying the median nerve) and S36–37 (overlying the deep peroneal nerve) reduced high blood pressure in a subset of patients (~70 %) with mild-to-moderate hypertension, in a slow-onset (4–8 weeks) but long-lasting (1–2 months) manner. EA inhibited cardiovascular sympathoexcitatory neurons through activation of neurons in the arcuate nucleus of the hypothalamus, the ventrolateral periaqueductal gray in the midbrain and the nucleus raphe pallidus in the medulla, through inhibiting the activity of premotor sympathetic neurons in the rostral ventrolateral medulla (rVLM). Several neurotransmitters such as glutamate, acetylcholine, opioids, GABA, nociceptin, serotonin and endocannabinoids were involved in this EA-induced hypotensive response. The long-lasting inhibition of hypertension induced by EA was related to opioids and GABA in the rVLM, neural circuitry between the arcuate and ventrolateral periaqueductal gray, and prolongation of the increase in preproenkephalin mRNA levels and enkephalin levels in the rVLM and arcuate. Moreover, the long-lasting inhibition of sympathetic activity by EA was confirmed in EA-treated hypertensive patients with decreased levels of norepinephrine, renin and aldosterone.