Dual receptor blockade by bosentan: clinical experience in treatment of pulmonary hypertension

Abstract

Pulmonary hypertension is characterized by an increase in mean pulmonary arterial pressure and right ventricular overload. Endothelin-1 (ET-1) is a potent vasoconstrictor with an important role in the pathogenesis of pulmonary hypertension. In addition to its vasoconstrictive action, ET-1 also stimulates cell proliferation, fibrosis, and inflammation. The blockade of both receptors involved in the action of ET-1 is beneficial in the treatment of pulmonary hypertension. The use of endothelin dual receptor blockade leads to improvements in quality of life, functional capacity, and pulmonary hemodynamics in affected patients. This article reviews the importance of ET-1 in the pathogenesis of pulmonary hypertension and demonstrates the benefits of blockage of the action of ET-1 in this disease.

Comparative Treatment Persistence and Adherence to Endothelin Receptor Antagonists Among Patients with Pulmonary Arterial Hypertension in Japan: A Real-World Administrative Claims Database Study

“…Five classes of agents that target these pathways are endothelin receptor antagonists (ERAs; e.g., macitentan, ambrisentan, and bosentan), phosphodiesterase type 5 (PDE5) inhibitors (e.g., sildenafil and tadalafil), prostanoids, selective prostacyclin receptor agonists, and soluble guanylate cyclase stimulators [2][3][4][5][6]. Bosentan was the first ERA to be synthesized and is a dual endothelin A and endothelin B receptor antagonist [7,8]. Ambrisentan is a selective endothelin A receptor antagonist [9], and macitentan is a dual endothelin A and endothelin B receptor antagonist [10,11].…”