NO and diabetic complications

摘要: Furchgott’s epochal discovery in 1980 of endothelium-dependent relaxation arteries by acetylcholine led to identification a labile material released endothelial cells first termed endothelium-derived relaxing factor and later shown be nitric oxide (NO). NO is now recognized as key mediator multiple physiologic processes that are perturbed diabetes. In induced diabetes the rat, for example, hypotensive response infusion sharply attenuated, perhaps due action advanced glycosylated endproducts. Another illustration impaired effect finding penile corpora cavernosa obtained from impotent diabetic men show total absence on exposure acetylcholine. While an exact role pathogenesis complications has yet defined, there no doubt it will. Therapeutic initiatives restore normal equilibrium rational objectives once pathophysiology elucidated.