- EA at LR3 reduced blood pressure and ameliorated behavioural abnormalities in mice with high-salt-induced hypertension.
- High salt exposure increased intrinsic excitability of PVN-RVLM and PVN-NTS projection neurons; EA normalised this neuronal hyperactivity.
- Proteomics revealed PVN mitochondrial remodelling with reduced ANT1/SLC25A4 expression in hypertension, restored by EA alongside reduced inflammatory and stress proteins.
Front Med (Lausanne). 2026 Oct 20;13:1955943. doi: 10.3389/fmed.2026.1955943. eCollection 2026.
ABSTRACT
BACKGROUND: High-salt-induced hypertension is associated with sympathetic overactivation, autonomic imbalance, and neurobehavioral abnormalities. The paraventricular nucleus (PVN) regulates autonomic output through projections to the rostral ventrolateral medulla (RVLM) and nucleus tractus solitarius (NTS). Although electroacupuncture (EA) has antihypertensive effects, its central mechanisms remain unclear. Mitochondrial dysfunction contributes to neurogenic hypertension, but the role of mitochondrial regulators such as adenine nucleotide translocator 1 (ANT1/SLC25A4) in PVN dysfunction remains unknown.
METHODS: Male C57BL/6J mice were exposed to 2% NaCl for 4 weeks to induce hypertension, followed by EA stimulation at the Taichong (LR3) acupoint for 3 weeks. Blood pressure, behavioral performance, PVN neuronal activity, and molecular alterations were assessed using tail-cuff measurement, behavioral tests, retrograde tracing combined with whole-cell patch-clamp recording, and TMT-based quantitative proteomics, as well as using Western blotting and immunofluorescence analyses.
RESULTS: High-salt exposure increased blood pressure and induced behavioral alterations. EA significantly reduced hypertension and improved behavioral abnormalities. High-salt exposure enhanced the intrinsic excitability of PVN-RVLM and PVN-NTS projection neurons, whereas EA normalized neuronal hyperactivity. Proteomic analysis revealed PVN remodeling involving mitochondrial oxidative phosphorylation, ATP/ADP transport, and transmembrane transport pathways. ANT1/SLC25A4 was downregulated in hypertensive mice but restored by EA, accompanied by reversal of inflammatory and stress-related protein alterations.
CONCLUSIONS: EA at LR3 reduced blood pressure and PVN neuronal hyperexcitability in mice with high-salt-induced hypertension. EA was also associated with normalization of mitochondrial-related proteomic changes and ANT1/SLC25A4 expression in the PVN. These findings identify ANT1-associated mitochondrial alterations as a potential molecular correlate of PVN dysfunction during EA treatment, but their causal contribution remains to be determined.
PMID:42978707 | PMC:PMC13727468 | DOI:10.3389/fmed.2026.1955943
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