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Oxidative stress is implicated in the pathology of pulmonary arterial hypertension PAH. Previously, we demonstrated that vardenafil, a phosphodiesterase-5 inhibitor, has potential as therapy for PAH, although the mechanism remained uncharacterized. Here, we aimed to determine baseline levels of oxidative stress in PAH and investigate whether vardenafil affects oxidative stress levels while improving PAH. Compared with baseline patients or untreated controls rats, vardenafil significantly reduced pulmonary vascular resistance and increased cardiac output CO. In rats, vardenafil suppressed proliferation and enhanced apoptosis of pulmonary artery smooth muscle cells, attenuating small pulmonary artery remodelling, and right ventricular hypertrophy.

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Address correspondence to: Jeffry G. Weers, Respira Therapeutics, Inc. Results: RT was generally safe and well tolerated at single doses of 0. The most common treatment-emergent adverse events were mild-to-moderate headaches. There was no evidence of pulmonary irritation or inflammation. Vardenafil was absorbed very rapidly after inhalation as RT, independent of dose level and number of doses administered.

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