Contrasting actions of endothelin ETA and ETB receptors in cardiovascular disease

Markus P. Schneider, Erika I. Boesen, David M. Pollock

Research output: Chapter in Book/Report/Conference proceedingChapter

198 Scopus citations

Abstract

First identified as a powerful vasoconstrictor, endothelin has an extremely diverse set of actions that influence homeostatic mechanisms throughout the body. Two receptor subtypes, ETA and ETB, which usually have opposing actions, mediate the actions of endothelin. ETA receptors function to promote vasoconstriction, growth, and inflammation, whereas ETB receptors produce vasodilation, increases in sodium excretion, and inhibit growth and inflammation. Potent and selective receptor antagonists have been developed and have shown promising results in the treatment of cardiovascular diseases such as pulmonary arterial hypertension, acute and chronic heart failure, hypertension, renal failure, and atherosclerosis. However, results are often contradictory and complicated because of the tissue-specific vasoconstrictor actions of ETB receptors and the fact that endothelin is an autocrine and paracrine factor whose activity is difficult to measure in vivo. Considerable questions remain regarding whether ETA-selective or nonselective ET A/ETB receptor antagonists would be useful in a range of clinical settings.

Original languageEnglish (US)
Title of host publicationAnnual Review of Pharmacology and Toxicology
EditorsArthur Cho
Pages731-759
Number of pages29
DOIs
StatePublished - Feb 23 2007

Publication series

NameAnnual Review of Pharmacology and Toxicology
Volume47
ISSN (Print)0362-1642

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Keywords

  • Chronic kidney disease
  • Heart failure
  • Pulmonary hypertension
  • Receptor localization

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology

Cite this

Schneider, M. P., Boesen, E. I., & Pollock, D. M. (2007). Contrasting actions of endothelin ETA and ETB receptors in cardiovascular disease. In A. Cho (Ed.), Annual Review of Pharmacology and Toxicology (pp. 731-759). (Annual Review of Pharmacology and Toxicology; Vol. 47). https://doi.org/10.1146/annurev.pharmtox.47.120505.105134