Abstract
In 1980, Furchgott and Zawadski [1] reported the dependency of the relaxing effect of acetylcholine on the intact vascular endothelium. The authors postulated that the vasodilation must be mediated by an unstable humoral factor, later known as the endothelium-derived relaxing factor (EDRF). In 1987, two independent research groups published results which implied that nitric oxide (NO) accounts for the vasodilatatory action of EDRF [2, 3]. The generation of endogenous NO is a result of oxidation of one of the two terminal guanidino nitrogen atoms of L-arginine within the endothelial cells. Subsequent division of the oxidized L-arginine into NO and citrulline occurs [3, 4]. This process is calcium- and calmodulin-dependent, and is catalyzed by an enzyme termed “intrinsic” or “constitutive” NO synthase [5–7]; pulsatile flow characteristics [8] and shear stress [9] stimulate the generation of NO by this NO synthase. Due to the lipophilic characteristic of the formed NO, it rapidly diffuses from the vascular endothelium to vascular smooth muscles. In smooth muscle cells NO binds to the soluble guanulate cyclase, enhances the conversion of magnesium guanosine triphosphate into cyclic guanosine monophosphate (cGMP), and, thus, exerts a relaxing effect by the induction of dephosphorylation of myosin light chain filaments [10]. Whereas normal blood pressure homeostasis is dependent on this basal NO synthesis [11, 12], inappropriate vasodilation or shock may occur due to cytokine- or endotoxin-induced overproduction of NO [13–15] which then is produced by an isoform of the NO synthase, the “inducible” NO synthase.
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Rossaint, R., Gerlach, H., Pappert, D. (1994). Inhalation of Nitric Oxide in Severe ARDS. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1994. Yearbook of Intensive Care and Emergency Medicine 1994, vol 1994. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-85068-4_12
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DOI: https://doi.org/10.1007/978-3-642-85068-4_12
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