Clin Exp Hypertens. 2026 Dec 31;48(1):2728373. doi: 10.1080/10641963.2026.2728373. Epub 2026 Sep 10.
ABSTRACT
BACKGROUND: Contemporary hypertension management increasingly emphasizes hypertension-mediated organ damage (HMOD) rather than blood pressure (BP) targets alone. Electroacupuncture (EA) has been studied mainly as a non-pharmacological antihypertensive intervention, but whether its reported organ-level effects reflect BP lowering or additional tissue-level mechanisms remains unclear.
METHODS: This narrative mechanistic review synthesized preclinical and clinical literature from PubMed, Web of Science, Scopus and CNKI to organize EA-related evidence within a dual-pathway framework distinguishing BP-dependent from candidate BP-independent mechanisms across the brain, heart, kidney and vasculature.
RESULTS: Preclinical evidence, mainly from spontaneously hypertensive rats, suggests that EA attenuates central sympathetic outflow, modulates brainstem-hypothalamic autonomic circuits, downregulates systemic and tissue renin-angiotensin-aldosterone system signaling, and reduces oxidative stress and inflammation. Organ-level evidence is graded moderate, and is the most developed of the four domains, for cardiac remodeling, including left ventricular hypertrophy and myocardial fibrosis; it is low-to-moderate for conduit-artery vascular changes and low for renal and cerebral effects. Across available studies, BP reduction and favorable organ-level changes occur together. No study has used BP-matched controls to isolate a BP-independent component, and no human trial with validated organ-specific HMOD endpoints was identified.
CONCLUSION: Current evidence supports a hypothesis-generating dual-pathway framework in which EA-related organ effects may arise through BP-dependent mechanisms and candidate BP-independent tissue-level pathways. However, BP-independent organ protection remains unproven and requires BP-matched preclinical designs and sham-controlled human trials using validated HMOD surrogate endpoints.
PMID:42720262 | DOI:10.1080/10641963.2026.2728373