[1] HODGKIN A L, HUXLEY A F. A quantitative description of membrane current and its application to conduction and excitation in nerve[J]. J Physiol, 1952, 117(4): 500-544.
[2] YOST C S. Potassium channels: basic aspects, functional roles, and medical significance[J]. Anesthesiology, 1999, 90 (4): 1186-1203.
[3] PATEL A J, HONORE E. Anesthetic-sensitive 2P domain K+ channels[J]. Anesthesiology, 2001, 95(4): 1013-1021.
[4] KUANG Q, PURHONEN P, HEBERT H. Structure of potassium channels[J]. Cell Mol Life Sci, 2015, 72(19): 3677-3693.
[5] NOMA A. ATP-regulated K+channels in cardiac muscle[J]. Nature, 1983, 305(5930): 147-148.
[6] INOUE I, NAGASE H, KISHI K, et al. ATP-sensitive K+ channel in the mitochondrial inner membrane[J]. Nature,1991, 352 (6332): 244-247.
[7] INAGAKI N, GONOI T, SEINO S. Subunit stoichiometry of the pancreatic beta-cell ATP-sensitive K+ channel[J]. Febs Lett, 1997, 409(2): 232-236.
[8] OLSON T M, TERZIC A. Human KATP channelopathies: diseases of metabolic homeostasis[J]. Pflugers Arch, 2010, 460 (2): 295-306.
[9] AGUILAR-BRYAN L, NICHOLS C G, WECHSLER S W, et al. Cloning of the beta cell high-affinity sulfonylurea receptor: a regulator of insulin secretion[J]. Science, 1995, 268(5209): 423-426.
[10] AGUILAR-BRYAN L, BRYAN J. Molecular biology of adenosine triphosphate-sensitive potassium channels[J]. Endocr Rev, 1999, 20(2): 101-135.
[11] TESTAI L, RAPPOSELLI S, MARTELLI A, et al. Mito-chondrial potassium channels as pharmacological target forcardioprotective drugs[J]. Med Res Rev, 2015, 35(3): 520-553.
[12] FLAGG T P, ENKVETCHAKUL D, KOSTER J C, et al.Muscle KATP channels: recent insights to energy sensing and myoprotection[J]. Physiol Rev, 2010, 90(3): 799-829.
[13] 唐性春, 胡刚, 汪海. ATP敏感性钾通道的分子生物学与药理学研究进展[J]. 解放军药学学报, 2001, 17(1): 30-35.
[14] ARDEHALI H, OROURKE B. Mitochondrial K channels in cell survival and death[J]. J Mol Cell Cardiol, 2005, 39(1): 7-16.
[15] 张凌云, 高宝安. 肺动脉平滑肌细胞与低氧性肺血管重塑形成机制[J]. 中国动脉硬化杂志, 2013, 21(2): 177-181.
[16] MAUBAN J R. Hypoxic pulmonary vasoconstriction: role of ion channels[J]. J Appl Physiol, 2004, 98(1): 415-420.
[17] 陈磊, 解卫平, 金宇, 等. 吡那地尔及二氮嗪对长期低氧大鼠肺动脉平滑肌KATP通道蛋白表达的影响[J]. 南京医科大学学报(自然科学版), 2008, 28(3): 308-311.
[18] 肖欣荣, 程德云, 陈文彬. ATP钾通道开放剂对大鼠慢性低氧性肺动脉高压的作用[J]. 中华结核和呼吸杂志, 2003, 26(2): 36-39.
[19] DUMAS J P, DUMAS M, SGRO C, et al. Effects of two K+ channel openers, aprikalim and pinacidil, on hypoxic pulmonary vasoconstriction[J]. Eur J Pharmacol, 1994, 263(1-2): 17-23.
[20] HU H L, ZHANG Z X, CHEN C S, et al. Effects of mitochondrial potassium channel and membrane potential on hypoxic human pulmonary artery smooth muscle cells[J]. Am J Respir Cell Mol Biol, 2010, 42(6): 661-666.
[21] ALBERICI L C, PAIM B A, ZECCHIN K G, et al. Activation of the mitochondrial ATP-sensitive K+ channel reduces apoptosis of spleen mononuclear cells induced by hyperlipidemia[J]. Lipids Health Dis, 2013, 12: 87.
[22] WANG T, ZHANG Z X, XU Y J, et al. 5-Hydroxydecanoate inhibits proliferation of hypoxic human pulmonary artery smooth muscle cells by blocking mitochondrial KATP channels[J]. Acta Pharmacol Sin, 2007, 28(10): 1531-1540.
[23] 李秋, 张丽萍, 舒鹰, 等. 5-羟基癸酸盐对慢性低氧大鼠肺动脉Kv1.5通道表达的影响[J]. 中国病理生理杂志, 2011, 27(1): 22-26.
[24] DONG L, LI Y, HU H, et al. Potential therapeutic targets for hypoxia-induced pulmonary artery hypertension[J]. J Transl Med, 2014, 12: 39.
[25] 李少民, 成少利, 万俊哲, 等. 二氮嗪防治低氧性肺动脉高压的作用机制[J]. 西安交通大学学报(医学版), 2007, 28(5): 566-568.
[26] FDA Drug Safety Podcast: FDA warns about a serious lung condition in infants and newborns treated with Proglycem (diazoxide)[R]. 2015.
http://www.fda.gov/Drugs/DrugSafety/DrugSafetyPodcasts/ucm455659.htm.
[27] SASAKI N, MURATA M, GUO Y, et al. MCC-134, a single pharmacophore, opens surface ATP-sensitive potassium channels, blocks mitochondrial ATP-sensitive potassium channels, and suppresses preconditioning[J]. Circulation,2003, 107(8): 1183-1188.
[28] HUANG X, ZOU L, YU X, et al. Salidroside attenuates chronic hypoxia-induced pulmonary hypertension via adenosine A2a receptor related mitochondria-dependent apoptosis pathway[J]. J Mol Cell Cardiol, 2015, 82: 153-166.