Cold exposure induces hemodynamic disturbances and promotes cardiovascular disease development primarily through activation of the sympathetic nervous system and renin-angiotensin-aldosterone system.
Abstract Cold exposure induces significant hemodynamic disturbances that contribute to increased morbidity and mortality from cardiovascular disease (CVD). This review explores the physiological and molecular mechanisms by which cold stress affects blood pressure regulation, vascular resistance, and wall shear stress (WSS), and how these alterations promote CVD development. Cold exposure elevates blood pressure primarily through activation of the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS). These neurohumoral pathways enhance vasoconstriction and increase blood viscosity, thereby elevating peripheral vascular resistance. Moreover, cold-induced alterations in WSS impair endothelial function, facilitate platelet aggregation, and accelerate atherosclerotic progression. Despite extensive evidence linking cold exposure to hemodynamic and vascular dysfunction, the precise molecular and integrative mechanisms remain incompletely understood. We propose that the SNS-RAAS axis represents a central regulatory pathway underlying cold-induced hemodynamic changes, warranting further investigation to clarify its contribution to cold-related cardiovascular pathology.
Wu et al. (2026) conducted a review in Cardiovascular disease. Cold exposure was evaluated. Cold exposure induces hemodynamic disturbances and promotes cardiovascular disease development primarily through activation of the sympathetic nervous system and renin-angiotensin-aldosterone system.