Commentary - Journal of Clinical Endocrinology Research (2025) Volume 8, Issue 1

Deciphering the mechanisms of stress-induced cardiovascular dysfunction.

Ewa Szczepanska-Sadowska ^*

Department of Experimental and Clinical Physiology, Medical University of Warsaw, Warsaw, Poland

Corresponding Author:

Ewa Szczepanska-Sadowska
Department of Experimental and Clinical Physiology
Medical University of Warsaw, Warsaw, Poland
E-mail: esz1s@amwaw.edu.pl

Received: 05-Apr-2024, Manuscript No. AAJCER-24-131476; Editor assigned: 07-Apr-2024, AAJCER-24-131476 (PQ); Reviewed: 20-Apr-2024, QC No. AAJCER-24-131476; Revised: 07-Apr-2025, Manuscript No. AAJCER-24-131476 (R); Published: 14-Apr-2025, DOI: 10.35841/AAJCER.8.1.179

Citation: Deciphering the mechanisms of stress-induced cardiovascular dysfunction. J Clin Endocrinol Res. 2025;8(1):179

Keywords

Cardiovascular diseases, Sympathetic nervous system, Endothelial dysfunction, Oxidative stress, Neurohormonal.

Introduction

Chronic exposure to stress has been linked to the development and progression of cardiovascular diseases, including hypertension, atherosclerosis, and myocardial infarction. The physiological response to stress involves the activation of the Sympathetic Nervous System (SNS) and the Hypothalamic-Pituitary-Adrenal (HPA) axis, leading to the release of stress hormones such as cortisol, adrenaline, and noradrenaline. While acute stress responses are adaptive and essential for survival, chronic stress can dysregulate cardiovascular homeostasis and contribute to the pathogenesis of CVD.

Mechanisms of stress-induced cardiovascular dysfunction

Autonomic imbalance: Prolonged activation of the SNS and suppression of parasympathetic activity lead to autonomic imbalance, characterized by increased heart rate, blood pressure, and cardiac output. This dysregulation of autonomic tone contributes to the development of hypertension and arrhythmias.

Endothelial dysfunction: Chronic stress disrupts endothelial function, impairing vasodilation and promoting vasoconstriction and inflammation. Endothelial dysfunction predisposes individuals to atherosclerosis and thrombosis, increasing the risk of cardiovascular events.

Inflammatory response: Stress-induced activation of the immune system results in the release of pro-inflammatory cytokines and chemokines. Chronic inflammation contributes to the progression of atherosclerosis, plaque instability, and myocardial damage.

Oxidative stress: Excessive production of Reactive Oxygen Species (ROS) in response to chronic stress overwhelms endogenous antioxidant defenses, leading to oxidative stress. Oxidative damage to cellular components exacerbates endothelial dysfunction and promotes myocardial remodeling and fibrosis.

Neurohormonal activation: Dysregulation of the HPA axis and increased release of cortisol and catecholamines have detrimental effects on the cardiovascular system. Cortisol promotes gluconeogenesis, insulin resistance, and sodium retention, contributing to metabolic syndrome and hypertension. Catecholamines exert direct effects on myocardial contractility and vascular tone, exacerbating cardiac dysfunction and remodeling.

Therapeutic implications

Targeting stress-induced cardiovascular dysfunction requires a multifaceted approach aimed at mitigating the physiological and psychological effects of stress. Lifestyle interventions such as exercise, relaxation techniques, and stress management programs have been shown to reduce stress-related cardiovascular risk. Pharmacological interventions targeting neurohormonal pathways, inflammation, and oxidative stress may also have therapeutic potential in preventing and treating stress-induced cardiovascular dysfunction.

Conclusion

Stress-induced cardiovascular dysfunction represents a complex interplay between psychological, neuroendocrine, and cardiovascular pathways. By elucidating the underlying mechanisms and identifying novel therapeutic targets, clinicians and researchers can develop effective strategies for mitigating the adverse cardiovascular effects of stress and improving patient outcomes.