Issue title: Selected Papers from 1st Meeting on “Cardiovascular Biology: Endothelial Cell in Health and Hypertension”, 30 June–1 July 2006, Prague, Czech Republic
Affiliations: Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA | Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Note: [] Corresponding author: Suzanne Oparil, MD, University of Alabama at Birmingham, 1034 Zeigler Research Building, 703 19th Street South, Birmingham, AL 35294. Tel.: +1 205 934 2580; Fax: +1 205 934 0424; E-mail: [email protected]
Abstract: Endothelin-1 (ET-1) is a powerful vasoconstrictor and mitogen that contributes to blood pressure elevation and related vascular remodeling and target organ damage. ET-1 also influences salt and water homeostasis through effects on the renin-angiotensin-aldosterone system and vasopressin, thus elevating blood pressure and increasing vascular tone. Circulating ET-1 levels are elevated in a variety of animal models of hypertension, particularly those that are salt-dependent, and in a subset of human hypertensives, i.e. African-Americans and those with renal dysfunction. ET type B receptors, which normally have vasodilator functions, mediate vasoconstriction in some hypertensives, and hypertensive African-American patients may have increased numbers of vasoconstrictor ET-B receptors in their vascular smooth muscle. Whether selective ET-A or combined ET-A/ET-B receptor antagonists are more efficacious in treating hypertension and related cardiovascular disease is controversial. ET antagonists have only modest BP lowering effects in the general population of essential hypertensives, but show promise in patients with severe, treatment resistant hypertension.
