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 potent...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 O2 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 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 inhibited through interaction with an unidentified O2 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. [展开更多
文摘血管平滑肌（VSM）细胞和内皮细胞（EC）都表达K^＋通道，微血管平滑肌细胞至少表达4种不同类别的K^＋通道，内向整流性钾通道[inward rectifier K^＋（KIR）channel]；ATP敏感性钾通道[（ATP—sensitive K^＋（KATP）channel]；电压门控式钾通道[vohage—gated K^＋（Kv）channel]；大电导钙激活钾通道[the large conductance，Ca^2＋-activated K K^＋（MaxiK，BKCa）channel]。
文摘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 O2 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 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 inhibited through interaction with an unidentified O2 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. [
