Functional impact of oxidative stress on distinct blood cell lineages: Implications for arterial hypertension

Blood is a specialized connective fluid tissue composed of plasma and cellular components. It circulates throughout the vascular system as a mixture of about 55% plasma and 45% blood cells, ensuring the maintenance of physiological homeostasis. The cellular fraction of blood mainly includes erythrocytes, leukocytes, and platelets, each originating from hematopoietic stem cells in the bone marrow through tightly regulated differentiation processes. Collectively, these cells contribute to essential biological functions, such as oxygen transport, immune defense, hemostasis, and tissue repair. In addition to their classical functions, blood cells actively interact with endothelial cells and circulating mediators, allowing them to participate in systemic responses to infection, injury, metabolic disturbances, and have emerged as key contributors to inflammatory and oxidative stress-related processes. Together, the coordinated activity and dysfunction of these circulating cells contribute significantly to the propagation of inflammatory responses and oxidative stress, processes that are increasingly recognized as central drivers in the pathophysiology of numerous chronic diseases, including cardiovascular disorders such as arterial hypertension. This review provides a comprehensive overview of how oxidative stress alters ENaC channel activity and adhesion protein function in megakaryocytes, erythrocytes, neutrophils, and platelets, highlighting shared mechanistic pathways that may contribute to vascular dysfunction and chronic inflammatory diseases.