[1] Shimoni Y. Inhibition of the formation or action of angiotensin II reverses attenuated K+ currents in type 1 and type 2 diabetes animals [J]. J Physiol, 2001, 537(Pt 1): 83-92. [2] Shimoni Y, Ewart HS, Severson D. Type I and II models of diabetes produce different modifications of K+ currents in rat heart: role of insulin [J]. J Physiol, 1998, 507 (Pt 2): 485-496. [3] Shimoni Y, Firek L, Severson D, et al. Short-term diabetes alters K+ currents in rat ventricular myocytes [J]. Circ Res, 1994, 74 (4): 620-628. [4] Shimoni Y, Light PE, French RJ. Altered ATP sensitivity of ATP-dependent K+ channels in diabetic rat hearts [J]. Am J Physiol, 1998, 275 (4 Pt 1): E568-576. [5] Shimoni Y, Severson D, Giles W. Thyroid status and diabetes modulate regional differences in potassium currents in rat ventricle [J]. J Physiol, 1995, 488 (Pt 3): 673-688. [6] Nichols CG, Ripoll C, Lederer WJ. ATP-sensitive potassium channel modulation of the guinea pig ventricular action potential and contraction [J]. Circ Res, 1991, 68 (1): 280-287. [7] Krause E, Englert H, Gogelein H. Adenosine triphosphatedependent K+ currents activated by metabolic inhibition in rat ventricular myocytes differ from those elicited by the channel opener rilmakalim [J]. Pflugers Arch, 1995, 429 (5): 625-635. [8] Yang BF, Luo DL, BAO LH, et al. Artemisinin blocks activating and slowly activating K+ current in guinea pig ventricular myocytes [J]. Acta Pharm Sin, 1998, 19 (3): 269-272. [9] Ai J, Gao HH, He SZ, et al. Effects of matrine, artemisinin, tetrandrine on cytosolic [Ca2+]i in guinea pig ventricular myocytes [J]. Acta Pharm Sin, 2001, 22 (6): 512-515. [10] Li BX, Yang BF, Zhou J, et al. Inhibitory effects of berberine on IK1, IK, and HERGchannels of cardiac myocytes [J]. Acta Pharm Sin, 2001, 22 (2): 125-131. [11] Lu Y, Yue L, Wang Z, et al. Effects of the diuretic agent indapamide on Na+, transient outward, and delayed rectifier currents in canine atrial myocytes [J]. Circ Res, 1998, 83 (2): 158-166. [12] Zhang Y, Han H, Wang J, et al. Impairment of human ether-a-go-go-related gene (HERG) K+ channel function by hypoglycemia and hyperglycemia. Similar phenotypes but different mechanisms [J]. J Biol Chem, 2003, 278 (12): 10417-10426. [13] Tani M. Mechanism of Ca++ overload in reperfused ischemic myocardium [J]. Ann Rev Physiol, 1990, 52: 543-559. [14] Shimoni Y, Light PE, French RJ. Altered ATP sensitivity of ATP-dependent K+ channels in diabetic rat hearts [J]. Am J Physiol, 1998, 275 (4 Pt 1): E568-576. [15] Smith JM, Wahler GM. ATP-sensitive potassium channels are altered in ventricular myocytes from diabetic rats [J]. Mol Cell Biochem, 1996, 158 (1): 43-51. [16] Li GR, Feng J, Yue L, et al. Evidence for two components of delayed rectifier K+ current in human ventricular myocytes [J]. Circ Res, 1996, 78 (4): 689-696. [17] Jonassen AK, Sack MN, Mjos OD, et al. Myocardial protection by insulin at reperfusion requires early administration and is mediated via Akt and p70s6 kinase cell-survival signaling [J]. Circ Res, 2001, 89 (12): 1191-1198. [18] Chattou S, Diacono J, Feuvray D. Decrease in sodium-calcium exchange and calcium currents in diabetic rat ventricular myocytes [J]. Acta Physiol Scand, 1999, 166 (2): 137-144. [19] Wang DW, Kiyosue T, Shigematsu S, et al. Abnormalities of K+ and Ca2+ currents in ventricular myocytes from rats with chronic diabetes [J]. Am J Physiol, 1995, 269 (4 Pt 2): H1288-1296. [20] Magyar J, Rusznak Z, Szentesi P, et al. Action potentials and potassium currents in rat ventricular muscle during experimental diabetes [J]. J Mol Cell Cardiol, 1992, 24 (8): 841-853. |