Sarcoidosis-associated pulmonary hypertension: a role for endothelin receptor antagonists?

2009 ◽  
Vol 3 (3) ◽  
pp. 99-101 ◽  
Author(s):  
Georgia G. Pitsiou ◽  
Dionysis Spyratos ◽  
Ioannis Kioumis ◽  
Afroditi K. Boutou ◽  
Chrysanthi Nakou ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Endothelin Receptor Antagonists ◽  
Endothelin Receptor ◽  
Receptor Antagonists

scholarly journals Pulmonary hypertension: reasonable selection of specific therapy

2018 ◽  
Vol 15 (1) ◽  
pp. 45-50
Author(s):  
N A Karoli ◽  
S I Sazhnova ◽  
A P Rebrov
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Structural Changes ◽  
Pulmonary Arteries ◽  
Endothelin Receptor Antagonists ◽  
Endothelin Receptor ◽  
Receptor Antagonists ◽  
Pulmonary Vasodilator ◽  
Pulmonary Arterial

Pulmonary hypertension is characterized with persistent increase in pulmonary vascular resistance leading to progressive worsening of right ventricular failure and death. The basis for pulmonary arterial hypertension is structural changes in pulmonary arteries and arterioles caused by endothelial dysfunction. Endothelin-1 is the main pathogenic trigger of pulmonary hypertension and potential target for therapeutic exposure. The efficacy of endothelin receptor antagonists is proved in various preclinical and clinical studies. In patients with pulmonary arterial hypertension, the efficacy of dual and selective endothelin receptor antagonists is comparable despite the varied activity against various receptors. Bosentan is the most widely used pulmonary vasodilator which improves exercise tolerance and decelerates disease progression.

scholarly journals Endothelin receptor antagonists for pulmonary hypertension in adult patients with sickle cell disease

2009 ◽  
Vol 147 (5) ◽  
pp. 737-743 ◽  
Author(s):  
Caterina P. Minniti ◽  
Roberto F. Machado ◽  
Wynona A. Coles ◽  
Vandana Sachdev ◽  
Mark T. Gladwin ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Adult Patients ◽  
Endothelin Receptor Antagonists ◽  
Endothelin Receptor ◽  
Cell Disease ◽  
Receptor Antagonists

scholarly journals Endothelin Receptor Antagonism: A New Era in the Treatment of Pulmonary Arterial Hypertension

2002 ◽  
Vol 1 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Richard N. Channick ◽  
Lewis J. Rubin
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Endothelin Receptor Antagonists ◽  
Endothelin Receptor ◽  
Receptor Antagonists ◽  
Double Blind ◽  
Beneficial Effects ◽  
Endothelin System ◽  
Pulmonary Arterial

Abstract The endothelin system has been extensively studied over the last several years. It is clear that endothelin-1 (ET-1) is a key mediator in pulmonary vascular biology and physiology. Abnormal increases in ET-1 production and decreased pulmonary clearance appear to play a major pathogenetic and perpetuating role in the pulmonary hypertensive process, through their vasconstrictive, smooth muscle cell proliferative and profibrotic effects. The degree of overexpression of ET-1 may correlate with the severity of pulmonary hypertension (PH). Advances in understanding the role of ET-1 in pulmonary hypertension have driven the development of endothelin receptor antagonists. One such agent, bosentan (Tracleer), is FDA approved for pulmonary arterial hypertension. Bosentan was approved following two randomized, placebo-controlled, double-blind studies that both showed marked improvement in exercise capacity after treatment with bosentan. The beneficial effects of bosentan appear to be sustained in most patients followed for as long as 22 months. Other uses for endothelin receptor antagonists are being examined, such as in combination with epoprostenol (Flolan) or in pediatric PH patients.

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