title: Endothelin-1 and hypertension: from bench to bedside.
abstract: Endothelin-1 (ET-1) exerts a wide range of biologic effects that can influence systemic blood pressure. Recent studies indicate that increased activity of the ET system in the vasculature, with resultant activation of primarily ET A receptors, can contribute to hypertension. In contrast, decreased production of ET-1 in the renal medulla, and reduced activation of collecting duct ET B receptors, can also elevate systemic blood pressure. Both ET A and combined A/B receptor blockers reduce blood pressure in hypertensive patients. Several important questions remain with respect to the ET system in hypertension, including how ET receptor antagonists will interact with other antihypertensive agents, which receptor subtypes should be targeted, and what the effect of ET blockade will be on hypertension-related end-organ damage as opposed to blood pressure alone.
authors: Division of Nephrology, University of Utah Health Sciences Center, 1900 East 30 North, Salt Lake City, UT 84132, USA. donald.kohan@hsc.utah.edu
authors: Donald E
authors: DE
authors: Kohan
mesh_terms: D001794:Blood Pressure; D019332:Endothelin-1 / Q000378:metabolism*; D016232:Endothelins / Q000037:antagonists & inhibitors; D006801:Humans; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D044022:Receptor, Endothelin A / Q000378:metabolism; D044023:Receptor, Endothelin B / Q000378:metabolism
chemical_list: D019332:Endothelin-1; D016232:Endothelins; D044022:Receptor, Endothelin A; D044023:Receptor, Endothelin B