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It is an understatement to say that blood pressure regulation is complex, especially in terms of long-term control. Redundancy abounds among the intricate balance of vascular, neural, and renal components. For the past 30 years, a major focus has been on elucidating how the endothelium contributes to vascular physiology and pathophysiology, with many investigators suggesting a link between endothelial dysfunction and hypertension. After Yanagisawa et al1 first described the endothelial-derived constricting factor, endothelin (ET) 1, many investigators assumed that the most potent vasoconstrictor thus far identified would play a critical role in maintaining systemic vascular resistance and, therefore, contribute to blood pressure regulation. However, 20 years later, we are still only beginning to understand its very complex yet significant role in this realm. The difficulty in understanding the ET system is attributed to numerous factors, including the following: (1) the opposing roles of ETA and ETB receptors to produce vasoconstriction and vasodilation, respectively, along with the occasional ETB-dependent vasoconstriction; (2) the irreversible nature of ligand binding to the ET receptors; (3) the localized nature of ET action such that plasma levels do not necessarily reflect synthesis but, rather, the balance of synthesis and clearance; (4) global knockout models for ET and its receptors result in lethal phenotypes; and (5) the relatively underinvestigated function of ET receptors in the peripheral nervous system that can influence vascular tone and blood pressure.Breakthrough evidence for the ET system in the control of blood pressure came from studies by Gariepy and collaborators,2,3⇓ who published several key articles revealing that genetic deficiency in ETB receptor function results in elevated blood pressure and salt-dependent hypertension. Mutation of the ETB receptor prevents development of the enteric nervous system, so animals homozygous for this trait develop megacolon and die …

Dissecting the Complex Physiology of Endothelin