Why the study?
To investigate the mechanism of electroacupuncture on sympathetic nerve activity and blood pressure reduction in the hypothalamic paraventricular nucleus of spontaneous hypertensive rats.
Does electroacupuncture reduce blood pressure and sympathetic nerve excitability in spontaneous hypertensive rats?
Does electroacupuncture reduce blood pressure and sympathetic nerve excitability in spontaneous hypertensive rats?
Electroacupuncture reduces blood pressure and sympathetic nerve excitability in hypertensive rats, potentially via inhibition of NMDAR-mediated Ang II/AT1 and inflammatory responses in the paraventricular nucleus.
Answers are grounded in this paper and cite their sources.
Electroacupuncture effects on BP in SHRs remain preliminary; leaves open clinical translation pending human studies.
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: 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.
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Sun et al. (2025) studied this question.
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