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 channels) are key to HPV: a change in the intracellular hydrogen peroxide (HO) levels during acute hypoxia is assumed to modulate these channels' activity to trigger HPV.
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