Titlebook: Endothelial Function in Hypertension; David Webb,Patrick Vallance Conference proceedings 1997 Springer-Verlag Berlin Heidelberg 1997 ather

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Endothelin Antagonists: Novel Treatments for Hypertension?,erived from the vascular endothelium (Yanagisawa et al. 1988). When administered intravenously in experimental animals or man ET-1 produces long-lasting increases in blood pressure (Yanagisawa et al.1988; Clarke et al.1989; Vierhapper et al.1990). ET-1 can also modulate blood pressure by potentiatio

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Endothelin in Hypertension: A Role in Vascular Hypertrophy?,ts. Endothelin-1 is the main endothelin produced by the endothelium. Plasma levels of immunoreactive endothelin are normal or only slightly increased in experimental or human hypertension. The responsiveness of blood vessels to endothelin-1 is normal or attenuated in experimental and human hypertens

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Endothelin in Congestive Heart Failure: Pathophysiology and Therapeutic Implications,mechanism of activation of ET in CHF probably is multifactorial and includes stimulation by factors such as Angiotensin II and tissue hypoxia. The functional significance of ET activation in CHF is currently being elucidated by the use of potent ET receptor antagonists. Such studies support the conc

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https://doi.org/10.1007/978-3-642-60811-7atherosclerosis; blood pressure; cardiovascular; endothelin; heart; heart failure; hypertension; physiology

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Steuerung als Element von Schulentwicklung,n of endothelium-dependent relaxation and the existence of the endothelium-derived relaxing factor (EDRF) were described [1]. Seven years later EDRF was identified as an inorganic gas, NO [2]. Now it is clear that neurones, smooth muscle cells, cardiac myocytes, white cells and platelets, as well as

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https://doi.org/10.1007/978-3-322-95122-9whether its production is or not affected in hypertension has been very controversial. Recent research work is showing the existence of profound differences in the role of NO in hypertension. This role seems to vary depending on the class of hypertension. In spontaneous and renovascular hypertension

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Erkenntnisinteresse und Herangehensweise,sease processes, simply by alterations in the quantity of nitric oxide released from endothelial cells (Cohen 1995). It is now clear that superoxide anion inactivates nitric oxide, that superoxide anion levels are a major determinant of nitric oxide activity and endothelial cell function, and that d

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https://doi.org/10.1007/978-3-658-18151-2ells lining the inner surfaces of the cardiac chambers. It is now recognised that these cardiac endothelial cells influence myocardial function through the paracrine release of a variety of diffusible substances (Shah 1996). The initial suggestion that endothelial cells influence myocardial function