Department of Medicine, Susan-Samueli Center for Integrative Medicine, University of California, Irvine, California 92697, USA.
Auton Neurosci. 2010 Oct 28;157(1-2):24-30. doi: 10.1016/j.autneu.2010.03.015. Epub 2010 May 5.
EA at P 5-6 and S 36-37 using low current and low frequency may be able to reduce elevated blood pressure in a subset of patients (∼70%) with mild to moderate hypertension. The effect is slow in onset but is long-lasting. Experimental studies have shown that EA inhibition of cardiovascular sympathetic neurons that have been activated through visceral reflex stimulation is through activation of neurons in the arcuate nucleus of the hypothalamus, vlPAG in the midbrain and NRP in the medulla, which, in turn, inhibit the activity of premotor sympathetic neurons in the rVLM. The arcuate also provides direct projections to the rVLM that contain endorphins. Glutamate, acetylcholine, opioids, GABA, nociceptin, serotonin and endocannabinoids all appear to participate in the EA hypotensive response although their importance varies between nuclei. Thus, a number of mechanisms underlying the long-lasting effect of EA on cardiovascular function have been identified but clearly further investigation is warranted.
使用低电流和低频率在 P 5-6 和 S 36-37 进行电刺激可能能够降低一部分（约 70%）轻中度高血压患者的血压升高。这种效果起效缓慢，但持续时间长。实验研究表明，电刺激通过内脏反射刺激激活的心血管交感神经元的抑制作用是通过激活下丘脑弓状核、中脑 vlPAG 和延髓 NRP 中的神经元来实现的，进而抑制 rVLM 中的前运动交感神经元的活动。弓状核还提供直接投射到 rVLM 的内啡肽。谷氨酸、乙酰胆碱、阿片类物质、GABA、孤啡肽、血清素和内源性大麻素似乎都参与了电刺激的降压反应，尽管它们在核团之间的重要性不同。因此，已经确定了电刺激对心血管功能的长期影响的一些机制，但显然需要进一步的研究。
