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

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Nitric Oxide and Hypertension: Physiology and Pathophysiology,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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Endothelial Alterations in Atherosclerosis: The Role of Nitric Oxide,ay be due to reduced NO synthesis and/or increased degradation. A reduction in NO activity favors vasoconstriction, platelet adherence and aggregation, monocyte adherence, and generation of superoxide anion. NO affects these processes by cyclic GMP-dependent and cyclic GMP-independent pathways. By r

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Endothelial Factors and Myocardial Function,ells 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

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Vascular Biology of the Endothelin System,he vascular relaxation to acetylcholine [2] and the subsequent identification of this factor as nitric oxide [3]. An additional important stimulus to the discovery of endothelin was the recognition that endothelial cells in culture generate and release a polypeptide vasoconstrictor factor into the b