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- Joseph R H Mauban, Carmelle V Remillard, and Jason X-J Yuan.
- Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California-San Diego, 9500 Gilman Dr., MC 0725, La Jolla, CA 92093-0725, USA.
- J. Appl. Physiol. 2005 Jan 1; 98 (1): 415-20.
AbstractAcute hypoxia induces pulmonary vasoconstriction and chronic hypoxia causes structural changes of the pulmonary vasculature including arterial medial hypertrophy. Electro- and pharmacomechanical mechanisms are involved in regulating pulmonary vasomotor tone, whereas intracellular Ca(2+) serves as an important signal in regulating contraction and proliferation of pulmonary artery smooth muscle cells. Herein, we provide a basic overview of the cellular mechanisms involved in the development of hypoxic pulmonary vasoconstriction. Our discussion focuses on the roles of ion channels permeable to K(+) and Ca(2+), membrane potential, and cytoplasmic Ca(2+) in the development of acute hypoxic pulmonary vasoconstriction and chronic hypoxia-mediated pulmonary vascular remodeling.
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