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Acute lung injury and its more severe form, acute respiratory distress syndrome (ARDS), are characterized by extensive alveolar injury and lung edema. It has been established that the resolution of ARDS parameters is highly dependent on alveolar regeneration and edema resorption. Because we previously demonstrated that KvLQT1 potassium channels are involved in alveolar repair processes and in the control of ion and liquid transports in vitro , we now decided to investigate their role in lung function and in the resolution of ARDS parameters in vivo , using a KvLQT1 knockout (KO) mice model. We first noted an absence of morphological difference in airway structures (trachea, bronchus and alveolus) between control (wild type, WT) and KvLQT1 KO mice. We then evaluated the impact of KvLQT1 extinction on the mechanical properties of the respiratory system using the flexiVent system (SCIREQ Inc.). Our results showed a significant increase of tissue damping and dynamic resistance of the respiratory system in KvLQT1 KO mice compared to WT. The role of KvLQT1 was then evaluated in a model of lung edema induced by thiourea, disrupting the integrity of endothelial/alveolar barrier. We observed a significant increase in the wet/dry ratio (W/D, index of lung edema) in both WT and KO mice. Interestingly, the thiourea‐induced W/D increase was partially prevented by a treatment with R‐L3, a KvLQT1 activator, in WT mice. However, this beneficial effect of R‐L3 was lost in KO mice. Our results show that the activation of KvLQT1 K + channels could play a role in the resolution of ARDS parameters, especially pulmonary edema resorption. Funded by CIHR, NSERC, FRQS.