Hypoxic pulmonary vasoconstriction (HPV) optimizes gas exchange but, when impaired, can result in life-threatening hypoxemia. Moreover, under conditions of generalized alveolar hypoxia, HPV can result in pulmonary hypertension. Voltage-gated K(+) channels (K(v) channels) are key to HPV: a change in the intracellular hydrogen peroxide (H(2)O(2)) levels during acute hypoxia is assumed to modulate these channels' activity to trigger HPV. However, there are longstanding conflicting findings on whether H(2)O(2) inhibits or activates K(v) channels. Therefore, we hypothesized that H(2)O(2) affects K(v) channels depending on the experimental conditions, i.e., the H(2)O(2) concentration, the channel's subunit configuration or the experimental clamping potential in electrophysiological recordings. Therefore, cRNAs encoding the K(v)1.5 channel and the auxiliary K(v)
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