Autonomic Nervous System Dysregulation in Metabolic Syndrome: An Association With Hypertension and Cardiovascular Risk

Scritto il 13/01/2026
da Hoor Soomra

Cureus. 2025 Dec 10;17(12):e98932. doi: 10.7759/cureus.98932. eCollection 2025 Dec.

ABSTRACT

Metabolic syndrome (MetS) is a cluster of cardiometabolic abnormalities, including abdominal obesity, insulin resistance, dyslipidemia, and elevated blood pressure, that increases the risk of type 2 diabetes and cardiovascular disease (CVD). Autonomic imbalance, characterized by increased sympathetic activity and reduced parasympathetic tone, is proposed to play an important role in the development of hypertension and adverse cardiovascular outcomes in individuals with MetS. This systematic review evaluates the association between autonomic nervous system (ANS) dysregulation and MetS. A systematic search was conducted in PubMed, Embase, Scopus, and Cochrane Library for studies published from January 2015 to September 2025. Eligible studies included human research that examined measures of autonomic function such as heart rate variability (HRV), baroreflex sensitivity, muscle sympathetic nerve activity, and plasma catecholamine levels at rest in individuals with MetS. Observational and interventional studies were included. Data were extracted and synthesized narratively. A total of 16 studies met the inclusion criteria. Most included studies reported reduced HRV, impaired baroreflex sensitivity, increased resting sympathetic nerve activity, and elevated plasma catecholamines in participants with MetS, suggesting a consistent association between ANS dysregulation and blood pressure elevation. However, causality could not be established due to the predominantly observational study designs. Current evidence indicates a significant association between autonomic dysfunction and MetS, particularly in relation to hypertension and increased cardiovascular risk. ANS biomarkers may support refined cardiometabolic risk stratification, although further prospective and mechanistic studies are needed to clarify causal pathways.

PMID:41527607 | PMC:PMC12790493 | DOI:10.7759/cureus.98932