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- Publisher
- Springer Journals
- Copyright
- Copyright © 2014 by Springer International Publishing Switzerland
- Subject
- Medicine & Public Health; Cardiology; Pharmacotherapy; Pharmacology/Toxicology
- ISSN
- 1175-3277
- eISSN
- 1179-187X
- DOI
- 10.1007/s40256-014-0095-y
- pmid
- 25421754
- Publisher site
- See Article on Publisher Site
Abstract
Pulmonary arterial hypertension (PAH) is a devastating life-threatening disorder characterized by elevated pulmonary vascular resistance leading to elevated pulmonary arterial pressures, right ventricular failure, and ultimately death. Vascular endothelial cells mainly produce and secrete endothelin (ET-1) in vessels that lead to a potent and long-lasting vasoconstrictive effect in pulmonary arterial smooth muscle cells. Along with its strong vasoconstrictive action, ET-1 can promote smooth muscle cell proliferation. Thus, ET-1 blockers have attracted attention as an antihypertensive drug, and the ET-1 signaling system has paved a new therapeutic avenue for the treatment of PAH. We outline the current understanding of not only the pathogenic role played by ET-1 signaling systems in the pathogenesis of PH but also the clinical pharmacology of endothelin receptor antagonists (ERA) used in the treatment of PAH.
Journal
American Journal of Cardiovascular Drugs – Springer Journals
Published: Nov 25, 2014