Effect of electroacupuncture on hypertensive and sympathetic excitability mechanism mediated by the paraventricular nucleus of the hypothalamus in spontaneous hypertensive rats.

Sun Jiao, Wang Yueming, Lyu Jian, Liu Xin, Yue Bingnan, L I Yinyin, Liu Jipeng, Sun Yize, Liu Qingguo, Yan Liu
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Abstract

Objective: To investigate the mechanism of electroacupuncture of sympathetic nerve activity and blood pressure reduction in the hypothalamic paraventricular nucleus (PVN) of spontaneous hypertensive rats (SHRs).

Methods: A total of 64 male SHRs were divided into four groups: model, sham-operated (Sham), electro-acupuncture (EA), and N-methyl-D-aspartate receptor antagonist and electroacupuncture (NRA + EA). In addition, 16 Wistar-Kyoto rats were used as controls. PVN stereotaxic surgery was performed in both the Sham and NRA + EA groups, while the EA and NRA + EA groups received 14 d of electroacupuncture. Blood pressure (BP) and heart rate (HR) were measured the day before the intervention and every other day. After 14 d of intervention, the rats in each group were tested for renal sympathetic nerve activity (RSNA). The associated factor levels were determined using Western blotting, reverse transcription-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA) and immunofluorescence assays.

Results: In comparison to the model group, the EA and NRA + EA groups had significantly lower BP, HR, and RSNA (P < 0.01). The expression of N-methyl-D-aspartate receptor (NMDAR), angiotensin II (Ang II), angiotensin II type 1 (AT1), tumor necrosis factor-α, interleukin-1β, norepinephrine and arginine vasopressin was significantly lower in the EA and NRA + EA groups (P < 0.01). Moreover, the antihypertensive effect of NRA+EA group outperformed to the EA group.

Conclusions: Electroacupuncture effectively reduced the BP and sympathetic nerve excitability in SHRs. The mechanism was linked to the inhibition of NMDAR-mediated Ang II /AT1 and the inflammatory response in PVN.

电针对自发性高血压大鼠高血压及下丘脑室旁核介导的交感兴奋性机制的影响。
目的:探讨电针对自发性高血压大鼠下丘脑室旁核(PVN)交感神经活动和血压降低的作用机制。方法:将64例男性SHRs分为模型组、假手术组(Sham)、电针组(EA)和n -甲基- d -天冬氨酸受体拮抗剂+电针组(NRA + EA)。另取Wistar-Kyoto大鼠16只作为对照。Sham组和NRA + EA组均行PVN立体定向手术,EA组和NRA + EA组均电针治疗14 d。在干预前一天和隔天测量血压(BP)和心率(HR)。干预14 d后,检测各组大鼠肾交感神经活性(RSNA)。采用Western blotting、逆转录聚合酶链反应(RT-PCR)、酶联免疫吸附法(ELISA)和免疫荧光法检测相关因子水平。结果:与模型组比较,EA组和NRA + EA组大鼠血压、HR、RSNA均显著降低(P < 0.01)。EA组和NRA + EA组n-甲基- d -天冬氨酸受体(NMDAR)、血管紧张素II (Ang II)、血管紧张素II 1型(AT1)、肿瘤坏死因子-α、白细胞介素-1β、去甲肾上腺素和精氨酸加压素的表达均显著降低(P < 0.01)。NRA+EA组降压效果优于EA组。结论:电针可有效降低SHRs的血压和交感神经兴奋性。其机制与nmdar介导的Ang II /AT1的抑制和PVN的炎症反应有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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