肺动脉平滑肌细胞氧敏感钾通道与低氧性肺血管收缩

Role of oxygen sensitive potassium channels in pulmonary arteries smooth muscle cells in hypoxic pulmonary vasoconstriction

The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of oxygen sensitive potassium channels open at the resting membrane potential in pulmonary arteries smooth muscle cells (PASMCs), so the oxygen sensitive potassium channels in PASMCS play a vital role in the occurrence and development of hypoxic pulmonary vasoconstriction (HPV). Inhibition the function of channels by specific antagons, Antibody-based dissection of the pulmonary arterial smooth muscle cell K+ current, the O2 sensitivity of cloned K+ channels expressed in heterologous expression systems and gene targeting to knockout specific K+ channels have all been examined to identify the molecular components of the pulmonary arterial O2-sensitive K+ channels. Although the mechanism of K+ channel inhibition by hypoxia is unknown, it appears that K+ α -subunits do not sense O2 directly. Rather, they are most likely inhibited through interaction with an unidentified O2 sensor and/or α-subunit. This review summarizes the role of K+ channels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of K+ channel subunits involved in this response, and the possible mechanisms of K+ channel regulation by hypoxia. [

The hypoxia - induced membrane depohu＇ization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of oxygen sensitive potassium channels open at the resting membrane potential i. pulmonary arteries smooth muscle cells （PASMCs）, so the oxygen sensitive potassium channels in PASMCS play a vital role in the occurrence and development of hypoxic pulmonary vasoconstriction （HPV）, Inhibition the function of channels hy specific antagons, Antibody -based dissection of the pulmonary arterial smooth muscle cell K^＋ current, the O2 sensitivity of cloned K^ ＋ channels expressed in heterologous expression systems and gene targeting to knockout specific K^＋ channels have all heen examined to identify the molecular components of the pulmonary arterial O2 -sensitive K^＋ channels, Although the mechanism of K^＋ channel inhibition by hypoxia is unknown, it appears that K^＋ α -subunits do not sense O2 directly. Rather, they are most likely inhihited through interaction with an unidentified O2 sensor and/or a -subunil. This review summarizes the role of K^ ＋ehannels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of K^ ＋ channel subunits involved in this response, and the possihle mechanisms of K^＋ channel regulation by hypoxia.