Nitric oxide: ocular blood flow, glaucoma, and diabetic retinopathy. Export

@article{citeulike:2855146, abstract = {Nitric oxide (NO) is widely recognized to be quite an important intercellular messenger in the cardiovascular and nervous systems or immunological reactions, including that in the eye. This molecule formed by constitutive NO synthase (NOS), endothelial (eNOS) and neuronal (nNOS), contributes to physiologically regulate ocular hemodynamics and cell viability and protects vascular endothelial cells and nerve cells or fibers against pathogenic factors associated with glaucoma, ischemia, and diabetes mellitus. Ocular blood flow is regulated by NO derived from the endothelium and efferent nitrergic neurons. Endothelial dysfunction impairs ocular hemodynamics by reducing the bioavailability of NO and increasing the production of reactive oxygen species (ROS). On the other hand, NO formed by inducible NOS (iNOS) expressed under influences of inflammatory mediators evokes neurodegeneration and cell apoptosis, leading to serious ocular diseases. NO over-produced by nNOS in the retina stimulated by excitotoxic amino acids or exposed to ischemia also mediates retinal injury. Because of these dichotomous roles of NO, which has both beneficial and pathogenic actions, one may face difficulties in constructing therapeutic strategies with NO supplementation or NOS inhibition. Up-to-date information concerning physiological roles of NO produced by the different NOS isoforms in the eye and interactions between NO and glaucoma, retinal ischemia, or diabetic retinopathy would help clinicians to select a valid pharmacological therapy that would be appropriate for a specific ocular disease.}, address = {Toyama Institute for Cardiovascular Pharmacology Research, 7-13, 1-Chome, Azuchi-machi, Chuo-ku, Osaka, Japan. n.toda.toyama-bldgy@orion.ocn.ne.jp}, author = {Toda, N. and Nakanishi-Toda, M.}, citeulike-article-id = {2855146}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.preteyeres.2007.01.004}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/17337232}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=17337232}, doi = {10.1016/j.preteyeres.2007.01.004}, issn = {1350-9462}, journal = {Progress in retinal and eye research}, keywords = {diabetic, glaucoma, retinopathy}, month = {May}, number = {3}, pages = {205--238}, posted-at = {2008-06-01 17:47:09}, priority = {2}, title = {Nitric oxide: ocular blood flow, glaucoma, and diabetic retinopathy.}, url = {http://dx.doi.org/10.1016/j.preteyeres.2007.01.004}, volume = {26}, year = {2007} }

TY - JOUR ID - citeulike:2855146 L3 - citeulike-article-id:2855146 N2 - Nitric oxide (NO) is widely recognized to be quite an important intercellular messenger in the cardiovascular and nervous systems or immunological reactions, including that in the eye. This molecule formed by constitutive NO synthase (NOS), endothelial (eNOS) and neuronal (nNOS), contributes to physiologically regulate ocular hemodynamics and cell viability and protects vascular endothelial cells and nerve cells or fibers against pathogenic factors associated with glaucoma, ischemia, and diabetes mellitus. Ocular blood flow is regulated by NO derived from the endothelium and efferent nitrergic neurons. Endothelial dysfunction impairs ocular hemodynamics by reducing the bioavailability of NO and increasing the production of reactive oxygen species (ROS). On the other hand, NO formed by inducible NOS (iNOS) expressed under influences of inflammatory mediators evokes neurodegeneration and cell apoptosis, leading to serious ocular diseases. NO over-produced by nNOS in the retina stimulated by excitotoxic amino acids or exposed to ischemia also mediates retinal injury. Because of these dichotomous roles of NO, which has both beneficial and pathogenic actions, one may face difficulties in constructing therapeutic strategies with NO supplementation or NOS inhibition. Up-to-date information concerning physiological roles of NO produced by the different NOS isoforms in the eye and interactions between NO and glaucoma, retinal ischemia, or diabetic retinopathy would help clinicians to select a valid pharmacological therapy that would be appropriate for a specific ocular disease. IS - 3 JF - Progress in retinal and eye research SN - 1350-9462 AD - Toyama Institute for Cardiovascular Pharmacology Research, 7-13, 1-Chome, Azuchi-machi, Chuo-ku, Osaka, Japan. n.toda.toyama-bldgy@orion.ocn.ne.jp EP - 238 TI - Nitric oxide: ocular blood flow, glaucoma, and diabetic retinopathy. VL - 26 SP - 205 KW - diabetic KW - glaucoma KW - retinopathy AU - Toda, N AU - Nakanishi-Toda, M PY - 2007/05// UR - http://dx.doi.org/10.1016/j.preteyeres.2007.01.004 ER -