The dysfunction of lung endothelium is crucial in the development of pulmonary hypertension. Dysfunction of endothelial synthesis of prostacyclin (PGI2) and nitric oxide (NO) and increased activity of endothelin 1 (ET-1) are connected to the progress of the disease. In this review the authors describe three major mediators of pulmonary endothelium: NO, PGI2 and ET-1. Their role in pulmonary hypertension and possibilities of pharmacological modulation of their activity are also discussed.
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