Hypoxia induces a pulmonary arterial pressor response by causing depolarization of pulmonary arterial smooth muscle cells through potassium loss and sodium gain.
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Highlights ionic mechanism of hypoxic vasoconstriction in animals; leaves open translation to human pulmonary hypertension.
The mechanisms underlying the pulmonary arterial pressor response to hypoxia have been investigated by studying specimens of pulmonary and systemic vascular smooth muscle and the isolated pulmonary and systemic circulations. Hypoxia caused a unique and reversible loss of potassium and gain in sodium by pulmonary arterial smooth muscle that did not occur in pulmonary veins or systemic arteries. These changes in electrolyte concentrations were calculated by the Nernst equation to be associated with depolarization of the smooth muscle cell of the pulmonary artery. Moreover, artificial hyperpolarization and depolarization in the isolated perfused pulmonary circulation were attended by blunting and accentuation, respectively, of the pulmonary arterial pressor response to hypoxia. Such data suggest that one of the actions of hypoxia on the pulmonary circulation involves a depolarization of the muscle cell so that it is closer to its excitatory threshold and thereby more readily able to diminish the cross-sectional area of the pulmonary vascular bed.
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Bergofsky et al. (1967) studied this question.
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