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Modulation of endothelin receptors in the failing right ventricle of the heart and vasculature of the lung in human pulmonary arterial hypertension.

Abstract：

AIMS:In pulmonary arterial hypertension (PAH), increases in endothelin-1 (ET-1) contribute to elevated pulmonary vascular resistance which ultimately causes death by right ventricular (RV) heart failure. ET antagonists are effective in treating PAH but lack efficacy in treating left ventricular (LV) heart failure, where ETA receptors are significantly increased. The aim was to quantify the density of ETA and ETB receptors in cardiopulmonary tissue from PAH patients and the monocrotaline (MCT) rat, which recapitulates some of the pathophysiological features, including increased RV pressure. MAIN METHODS:Radioligand binding assays were used to quantify affinity, density and ratio of ET receptors. KEY FINDINGS:In RV from human PAH hearts, there was a significant increase in the ratio of ETA to ETB receptors compared with normal hearts. In the RV of the MCT rat, the ratio also changed but was reversed. In both human and rat, there was no change in LV. In human PAH lungs, ETA receptors were significantly increased in the medial layer of small pulmonary arteries with no change detectable in MCT rat vessels. SIGNIFICANCE:Current treatments for PAH focus mainly on pulmonary vasodilatation. The increase in ETA receptors in arteries provides a mechanism for the beneficial vasodilator actions of ET antagonists. The increase in the ratio of ETA in RV also implicates changes to ET signalling although it is unclear if ET antagonism is beneficial but the results emphasise the unexploited potential for therapies that target the RV, to improve survival in patients with PAH.

journal_name

Life Sci

journal_title

Life sciences

authors

Kuc RE,Carlebur M,Maguire JJ,Yang P,Long L,Toshner M,Morrell NW,Davenport AP

doi

10.1016/j.lfs.2014.02.020

subject

Has Abstract

pub_date

2014-11-24 00:00:00

pages

391-6

issue

2

eissn

0024-3205

issn

1879-0631

pii

S0024-3205(14)00262-8

journal_volume

118

pub_type

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