Differential associations of oxidative stress parameters with neuroendocrine markers and hemodynamic reactivity in acute mental stress-induced adrenergic reactivity profiles: The SABPA study.

Stress-induced alpha (α)- and beta (β)-adrenergic reactivity profiles relate to distinct neuroendocrine-associated hemodynamic reactivity and cardiometabolic risk profiles. While oxidative stress links stress to cardiometabolic risk, its relationship with neuroendocrine markers and hemodynamics remains unclear. Within these profiles, we investigated resting oxidative stress parameters and their associations with neuroendocrine markers and hemodynamic reactivity. We included 362 participants (aged 20-65 years) and recorded beat-to-beat hemodynamic reactivity during the Stroop-Color-Word-Conflict test. We categorized α-responders (n = 47), β-responders (n = 68) and mixed-α/β-responders (n = 247) based on cardiac output (∆%CO) and Windkessel arterial compliance (∆%Cwk) reactivity. Baseline fasting urine and blood samples were analyzed for neuroendocrine markers and oxidative stress parameters. Predominant α-responders were older with higher hypertension prevalence than other responders. Oxidative stress parameters were comparable between α- and β-responders. In α-responders, SOD and GR inversely associated with ∆%CO and GPx positively with ∆%Cwk (all p ≤ 0.026). In β-responders, u-NE/Cr positively associated with GGT, ACTH inversely with ROS and tGSH positively with ∆%CO (all p ≤ 0.014). Our findings highlight divergence in cardiometabolic risk pathways. In α-responders, enzymatic antioxidants may support downstream vascular hemodynamic buffering in response to high-pressure-related vascular risk. In β-responders, sympathetic-driven increases in glutathione turnover could reflect antioxidant adaptation to preserve cardiac function during acute stress.