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Endothelial function mediators are a diverse group of signaling molecules produced by the vascular endothelium that play a critical role in maintaining vascular homeostasis. These mediators include vasodilators such as nitric oxide (NO), prostacyclin (PGI2), and endothelium-derived hyperpolarizing factors (EDHF), as well as vasoconstrictors like endothelin-1 (ET-1) and angiotensin II (Sena et al., 2018). Under physiological conditions, they regulate vascular tone, inhibit platelet aggregation, and modulate inflammatory responses. Endothelial dysfunction, characterized by an imbalance in these mediators—typically reduced NO bioavailability and increased ET-1—is a key early event in the pathogenesis of cardiovascular diseases, including atherosclerosis, hypertension, and heart failure (Poredos, 2021). Therapeutic strategies often target these mediators or their receptors to restore vascular function, such as using NO donors, endothelin receptor antagonists, or phosphodiesterase inhibitors. Because this term refers to a broad functional class of molecules rather than a single protein or receptor, it is not classified as a specific therapeutic target in isolation. Monitoring these mediators, such as measuring plasma endothelin-1 or nitric oxide metabolites, serves as a biomarker for vascular health and treatment efficacy (NIH, 2021). Overall, these mediators are central to the regulation of blood flow and the prevention of thrombotic and inflammatory vascular events.
Modulation of vascular tone through the donation of nitric oxide, antagonism of endothelin receptors, inhibition of phosphodiesterase-5, or inhibition of the renin-angiotensin system.
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