Role of bradykinin and endothelin-converting enzyme-1 in pulmonary hypertension

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By histological analysis, pulmonary vascular remodeling induced by MCT was also inhibited (vessel wall thickness: MCT 0.44 vs. M/A 0.31, p b 0.001). MCT treatment increased mRNA levels of endothelin (ET) receptor-A, ET receptor-B, ET-1 and transforming growth factor (TGF)beta in the lung. ADRCs therapy suppressed these increased mRNA (p b 0.05). Conclusion ADRC therapy inhibited the development of PAH by reversing the changes in ET expression and inflammatory cytokines. These findings suggest that ADRC therapy may open a novel strategy to treat PAH.

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