Titlebook: Relaxing and Contracting Factors; Biological and Clini Paul M. Vanhoutte Book 1988 The Humana Press Inc. 1988 Dilatation.Drogen.blood vesse

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Endothelium-Dependent Contractions in Veins and Arteries,in, the author’s laboratory discovered that the endothelial cells not only play an obligatory role in a number of dilator responses (Furchgott and Zawadzki, 1980; Furchgott, 1983, 1984; Vanhoutte et al., 1986), but also can induce contractions of isolated blood vessels when exposed to certain stimul

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The Nature of Endothelium-Derived Relaxing Factor, demonstrated in a wide range of blood vessels from a variety of species studied, including human (for reviews, see Furchgott, 1983; Griffith et al., 1985a; Busse et al., 1985). Endothelium-dependent relaxation can be elicited in vivo (Angus et al., 1983) as well as in standard in vitro pharmacologi

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Modulation of the Release and Biological Activity of Endothelium-Derived Relaxing Factor by Oxygen-mediates (oxygen-derived free radicals, Fig. 1), or quadrivalently by the mitochondrial cytochrome oxidase system, which avoids these reactive intermediates (DelMaestro, 1980; Freeman and Crapo, 1982). The presence and uniquity of enzymes (superoxide dismutase, catalase, and peroxidases) that scaven

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Endothelial Cells in Culture and Production of Endothelium-Derived Relaxing Factor,ical studies in which chemicals with diverse properties have been used to modify the relaxation caused by agonists releasing EDRF. Therefore any conclusions based on these approaches should necessarily be viewed with caution.

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Basal Release of Endothelium-Derived Relaxing Factor, and is active tonically in certain blood vessels. Release of EDRF elicited by chemical (e.g., acetylcholine) or physical (shear stress) stimuli is not discussed, nor is the release of prostacyclin, another endothelium-derived vasodilator, although this also occurs spontaneously (Gimbrone and Alexan

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Calcium Transport Mechanisms in Endothelial Cells Regulating the Synthesis and Release of Endothelition coupling in neurons and endocrine cells. Endothelium-dependent relaxation of blood vessels in response to numerous pharmacological [e.g., acetylcholine, adenosine diphosphate (ADP), and so on] and physiological (e.g., increase in flow) stimuli is mediated by a still-unidentified substance (“end

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Role of Cyclic GMP in Endothelium-Dependent Relaxation of Vascular Smooth Muscle, such as sodium nitroprusside, sodium azide, and nitroglycerin (Diamond and Blisard, 1976; Katsuki and Murad, 1977; Schultz et al., 1977); (2) contractile agents (Diamond and Blisard, 1976; Katsuki and Murad, 1977; Schultz et al., 1977); (3) atrial natriuretic factor (Winquist et al., 1984; Rapoport