Cytokine regulation of inducible nitric oxide synthase

Cohen, J., Evans, T.J. and Keith, I.A. (1997) Cytokine regulation of inducible nitric oxide synthase. In: Vincent, J.L. (ed.) Yearbook of Intensive Care and Emergency Medicine. Springer. ISBN 3540620818 (doi: 10.1007/978-3-662-13450-4_20)

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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].

Item Type:Book Sections
Glasgow Author(s) Enlighten ID:Evans, Professor Tom
Authors: Cohen, J., Evans, T.J., and Keith, I.A.
College/School:College of Medical Veterinary and Life Sciences > School of Infection & Immunity
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