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Myocardial effects of endothelin-1 [Efeitos miocárdicos da endotelina-1]

Title
Myocardial effects of endothelin-1 [Efeitos miocárdicos da endotelina-1]
Type
Another Publication in an International Scientific Journal
Year
2008
Authors
Bras Silva, C
(Author)
FCNAUP
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Leite Moreira, AF
(Author)
FMUP
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Journal
Vol. 27 No. 78
Pages: 925-951
ISSN: 0870-2551
Indexing
Publicação em ISI Web of Knowledge ISI Web of Knowledge
Other information
Authenticus ID: P-007-NN0
Abstract (EN): Endothelin (ET)-1 was originally identified in 1988 as a vasoconstrictor peptide produced by vascular endothelial cells. It is now known that ET-1 can be produced by vascular and endocardial endothelium and by myocardial cells. Activation of endothelin receptors modulates a wide variety of biological processes including vascular tone, growth and myocardial contractile function. In mammals, ET-1's effects are mediated through binding to two types of receptors, ETA and ETB. ETA receptor activation elicits vasoconstriction, positive inotropism and mitogenesis, and acutely increases myocardial distensibility. ETB receptor stimulation generally promotes vasodilatation, mediated by release of nitric oxide and prostacyclins, growth-inhibitory effects and clearance of ET-1 from the circulation. ETB receptors can be further subdivided into ET B1, located in endothelial cells and responsible for vasodilatation and negative inotropic effects, and ETB2, located in smooth muscle and myocardial cells and responsible for vasoconstriction and positive inotropic effects. Increased levels of cardiac and circulating ET-1 have been linked to development of cardiac dysfunction and severity of heart failure. This has fueled research into the development of endothelin antagonists (ET receptor and converting enzyme inhibitors) in view of the potential benefits that might derive from their use in clinical practice. The present review will focus on current understanding of the mechanisms mediating the myocardial actions of ET-1.
Language: English
Type (Professor's evaluation): Scientific
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