Mauban Joseph R H, Remillard Carmelle V, Yuan Jason X-J
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 (1985). 2005 Jan;98(1):415-20. doi: 10.1152/japplphysiol.00732.2004.
Acute 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.
急性缺氧会诱发肺血管收缩,而慢性缺氧则会导致肺血管结构改变,包括动脉中层肥厚。电机制和药理机械机制参与调节肺血管舒缩张力,而细胞内钙离子作为调节肺动脉平滑肌细胞收缩和增殖的重要信号。在此,我们对缺氧性肺血管收缩发生发展过程中涉及的细胞机制进行基本概述。我们的讨论聚焦于钾离子和钙离子通透性离子通道、膜电位以及细胞质钙离子在急性缺氧性肺血管收缩和慢性缺氧介导的肺血管重塑发生发展过程中的作用。