Titlebook: Endothelin and Its Inhibitors; Timothy D. Warner Book 2001 Springer-Verlag Berlin Heidelberg 2001 Circulation.Endothelin.Glatte Muskulatur

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https://doi.org/10.1007/978-3-322-97136-4ficient gas exchange. One critical aspect of pulmonary vascular physiology is the ability of the lung circulation to adapt to large variations in cardiac output with minimal impedance to blood flow at all levels (Voelkel and Weir 2000). In patients with PH, this ability is compromised, usually becau

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,Die ?konomisierung der Sozialen Arbeit,ctile responses that were both sustained and extremely resistant to wash-out (Yanagisawa et al. 1988). Subsequently, ET-1 has been shown to contract both resistance arterioles and venous tissue in addition to conduit arteries (venous tissue generally being more sensitive than arterial vessels; Brain

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,Soziale Arbeit – was ist das eigentlich?,(GI) smooth muscle preparations, and the relationships of these responses to the expression (mRNA), synthesis, production, and degradation of the endothelins and the distribution of ET receptors. Attention is also given to the possible physiological and pathophysiological roles of ETs in the gastroi

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https://doi.org/10.1007/978-3-658-32100-0d by a variety of cell types within the kidney including vascular and glomerular endothelium, mesangial cells and tubular epithelial cells. Sites of synthesis are in close proximity to receptors. ET-1 can produce a variety of responses through both ET. and ET. receptor subtypes located throughout th

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0171-2004 xicology of endothelin antagonists and endothelin-converting enzyme inhibitors, with mention of all the important members of these drug classes. This leads to well-rounded discussions of the potential therapeutic benefit of endothelin inhibitors.978-3-642-63237-2978-3-642-56899-2Series ISSN 0171-2004 Series E-ISSN 1865-0325

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,Digitale Handlungsf?higkeit Erringen,f tissue), whereas the SRTXs are produced in large amounts in the venom of the snake (0.1 mmol/g). The SRTXs and ETs may be divided into two groups on the basis of their toxicity. The most lethal are ET1 and SRTX-b; ET-3 is less toxic, and SRTX-c and SRTX-e cause death only at very high doses, if at

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Erich Schild,Rainer Oswald,Reinhard LamersECE) was proposed (Yanagisawa et al. 1988). Most studies have concluded that proendothelin-1 is processed intracellularly to ET-1 prior to its release (Corder et al. 1995b; Harrison et al. 1993, 1995; Russell and Davenport 1999; Xu et al. 1994). This is also the case for ET-2 (Lambert et al. 2000),

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