Research progress on the mechanisms linking obstructive sleep apnea and hypertension: a multidimensional exploration from hypoxia stress to metabolic dysregulation

Obstructive sleep apnea is a chronic disorder marked by intermittent hypoxia, which can lead to hypercapnia and decreased oxygen saturation. It is strongly correlated with a variety of cardiovascular diseases, particularly hypertension, although the fundamental molecular mechanisms have not been fully elucidated. This comprehensive narrative review summarizes the mechanisms via which obstructive sleep apnea promotes the pathogenesis of hypertension, including: reduced endogenous hydrogen sulfide levels leading to enhanced sympathetic activation and increased catecholamine synthesis; abnormal aminothiol metabolism and activation of the renal aryl hydrocarbon receptor signaling pathway; endothelial dysfunction induced by reactive oxygen species and inflammatory factors; synergistic effects of insulin resistance and metabolic syndrome; activation of the renin–angiotensin–aldosterone system and the hypothalamic–pituitary–adrenal axis, resulting in elevated aldosterone and cortisol levels; hemodynamic changes related to central venous pressure and intracranial pressure; cerebrovascular alterations associated with rapid eye movement sleep, and disruption of gut microbiota and how their metabolites modulate vascular homeostasis. Furthermore, this article also specifically discusses the sex differences in hypertension related to OSA. Collectively, these pathways untangle the complex relationship between obstructive sleep apnea and hypertension, providing a theoretical foundation for future mechanistic studies and potential avenues for the development of targeted treatment plans.