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Cytokine Regulation of Inducible Nitric Oxide Synthase

  • J. Cohen
  • T. J. Evans
  • L. A. Keith
Conference paper
  • 90 Downloads
Part of the Yearbook of Intensive Care and Emergency Medicine book series (YEARBOOK, volume 1997)

Abstract

A number of different lines of research have revealed the important roles that nitric oxide (NO) plays in mammalian cell biology. Since 1977 it has been known that NO activates soluble guanylate cyclase, producing a rise in intracellular cyclic guanosine monophosphate (cGMP) [1]. This in turn could produce vascular smooth muscle cell relaxation, and accounted for the vasorelaxatory properties of a number of different compounds such as organic nitrates and sodium nitroprusside [2, 3]. The mechanism of action of other vasodilators which did not themselves generate NO remained obscure, but was shown to be dependent on an intact endothelium, leading to the concept of an endothelium-derived relaxing factor (EDRF) [4]. Further work by two groups led to the discovery that the chemical nature of EDRF was in fact NO, or a closely related oxide of nitrogen [5, 6]. Subsequently, NO was found to be of key importance in vasodilatation and macrophage killing of microorganisms and tumor cells, and that NO is important in mediating a diverse number of biological effects, including acting as a neurotransmitter in non-adrenergic, non-cholinergic nerves [7], inhibiting platelet [8], and acting as a negative inotrope and chronotrope [9].

Keywords

Nitric Oxide Nitric Oxide Flavin Adenine Dinucleotide Flavin Adenine Dinucleotide Vasorelaxatory Property 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • J. Cohen
  • T. J. Evans
  • L. A. Keith

There are no affiliations available

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