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NO and diabetic complications

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Diabetic Renal-Retinal Syndrome

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Abstract

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

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Authors
  1. Robert F. Furchgott
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Editors and Affiliations

  1. Department of Medicine, State University of New York, Health Science Center at Brooklyn, Brooklyn, NY, USA

    Eli A. Friedman M.D. (Distinguished Teaching Professor) (Distinguished Teaching Professor)

  2. College of Physicians and Surgeons, Columbia University, New York, NY, USA

    Francis A. L’Esperance Jr. M.D. (Clinical Professor of Opthalmology) (Clinical Professor of Opthalmology)

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© 1998 Springer Science+Business Media Dordrecht

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Furchgott, R.F. (1998). NO and diabetic complications. In: Friedman, E.A., L’Esperance, F.A. (eds) Diabetic Renal-Retinal Syndrome. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4962-4_15

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  • DOI: https://doi.org/10.1007/978-94-011-4962-4_15

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-6083-7

  • Online ISBN: 978-94-011-4962-4

  • eBook Packages: Springer Book Archive

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