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Role of Nitric Oxide in Vascular Dysfunction Associated with Ocular Diseases

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Advances in Ocular Toxicology
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Abstract

Nitric oxide (NO) has emerged as a small, membrane-permeable free radical modulating numerous physiological functions in the cardiovascular, immune, and nervous systems1-5Within the cardiovascular system NO, originally described as endothelium derived relaxing factor, is released by a variety of agonists and cytokines as well as by pulsatile flow and shear stress, and is an important physiological modulator of systemic vascular tone and intravascular fluid volume67. Vascular NO functions constitutively to prevent adhesion of platelets and leukocytes and platelet aggregation thereby modulating coagulation and fibrinolyis. In addition, NO affects vascular function by modulating endothelial cell barrier function and vascular smooth muscle proliferation. Derangements in NO production have been linked to a variety of vascular pathologies including septic shock, hypertension, atherosclerosis, acute inflammation, and diabetes mellitus, and the overproduction of NO has been implicated in the pathogenesis of a number of autoimmune diseases.

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Tilton, R.G. (1997). Role of Nitric Oxide in Vascular Dysfunction Associated with Ocular Diseases. In: Green, K., Edelhauser, H.F., Hackett, R.B., Hull, D.S., Potter, D.E., Tripathi, R.C. (eds) Advances in Ocular Toxicology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5937-5_17

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