| Popis: |
Endothelial dysfunction is characterized by a reduction in nitric oxide generation or an unbalanced distribution of the relaxing and contracting pressures produced by endothelial cells. Endothelium was once assumed to be nothing more than a mechanical barrier. Endothelium is now recognized as a tissue that regulates tone, cell formation, leukocyte, thrombocyte, and artery wall contact. The pathophysiologic pathways behind endothelial dysfunction are of great interest, and researchers are working hard to figure out what they are and how they affect diabetes, psoriasis, Inflammatory Bowel Disease, hypertension, heart failure, renal failure, inflammation, stroke, atherosclerosis, and oxidative stress. Inflammatory activation and endothelial dysfunction are important processes in the progression and pathogenesis of atherosclerosis. Endothelial dysfunction in psoriasis patients with arterial hypertension is thought to be caused by a disturbance in the action of L-oxidative arginine's metabolism, as revealed by a decrease in NO bioavailability and a high degree of inactivation, oxidative stress, and an antioxidant state. The failing heart is characterised by irregular cardiac and vascular characteristics caused by abnormalities in NO bioavailability and oxidative stress. In such conditions the bioavailability of the NO can be increased by the various approaches like by using the NO generating compounds which can be done by either through inhalation of NO, use of the hybrid drugs like oral NO-NSAIDs combination or the use of inorganic nitrites. On other hand the endogenous NO levels can be increased by direct delivery of l‑arginine, l‑citrullineor Arginase inhibition. eNOS also can be activated by the use of statins, Corticosteroids, and Second generation β-adrenoceptor antagonists to increase NO level. This review will assist in understanding endothelial dysfunction, its pathogenesis, and its connection to a variety of disorders. |
