These results may be explained by 1) ET-1 secreted by endothelial cells in the culture medium contributes to vasoconstriction [37]; 2) the existence of ETA receptor in the spastic vessels [7]; 3) the dual “vasodilator-vasoconstrictor” role of ETB receptors as described in pulmonary vessels [38,39]; 4) the heterodimerization of ET receptors described in pulmonary hypertension [38]. This evidence concerns the gene EDN1 and pulmonary arterial hypertension.