| Title | Persistent sodium current and Na+/H+ exchange contributes to the augmentation of the reverse Na+/Ca2+ exchange during hypoxia or acute ischemia in ventricular myocytes |
| Authors | Tang, Qiong Ma, Jihua Zhang, Peihua Wan, Wei Kong, Linghao Wu, Lin |
| Affiliation | Wuhan Univ Sci & Technol, Coll Med, Cardio Electphysiol Res Lab, Wuhan 430081, Hubei, Peoples R China. Peking Univ, First Hosp, Dept Cardiol, Beijing 100871, Peoples R China. |
| Keywords | Hypoxia Sodium-calcium exchange current Persistent sodium current Sodium-hydrogen exchange Patch-clamp techniques ISOLATED CARDIAC MYOCYTES GUINEA-PIG HYDROGEN-PEROXIDE CALCIUM EXCHANGE NITRIC-OXIDE HIPPOCAMPAL-NEURONS HEART-CELLS INJURY INHIBITION ANOXIA |
| Issue Date | 2012 |
| Publisher | pflugers archiv european journal of physiology |
| Citation | PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY.2012,463,(4),513-522. |
| Abstract | The increases in persistent sodium currents (I (Na.P)) and Na+/H+ exchange (NHE) causes intracellular Ca2+ overload. The objective of this study was to determine the contribution of I (Na.P) and NHE on the hypoxia- or acute ischemia-induced increase in the reverse Na+/Ca2+ exchange current (HIR- or AIR-I (NCX)). I (Na.P) and I (NCX) in rabbit ventricular myocytes were recorded during hypoxia or acute ischemia, combination of acidosis (pH values were 6.0 intracellularly and 6.8 extracellularly) and hypoxia, using whole-cell patch-clamp techniques. The results indicate that (1) under hypoxic condition, the augmentation of both HIR-I (NCX) and I (Na.P) was inhibited by TTX (2 to 8 mu M) in a concentration-dependent manner. The inhibitions of I (Na,P) and HIR-I (NCX) reached maximum in the presence of either 4 mu M TTX or 10 mu M KR-32568 (a NHE inhibitor), respectively. The maximal inhibitions of HIR-I (NCX) by 4 mu M TTX and 10 mu M KR-32568 were 72.54% and 16.89%, respectively. (2) Administration of 2 mu M TTX and 10 mu M KR-32568 in either order in the same cells decreased HIR-I (NCX) by 64.83% and 16.94%, respectively. (3) I (Na.P) and the reverse I (NCX) were augmented during acute ischemia. TTX (4 mu M) and KR-32568 (10 mu M) reduced AIR-I (NCX) by 73.39% and 24.13%, respectively. (4) Under normoxic condition, veratridine (20 mu M) significantly increased I (Na.P) and the reverse I (NCX), which was reversed by 4 mu M TTX. In conclusion, during hypoxia or acute ischemia, both increased I (Na.P) and NHE contribute to the HIR- or AIR-I (NCX) with the former playing a major role comparing with the latter. |
| URI | http://hdl.handle.net/20.500.11897/393539 |
| ISSN | 0031-6768 |
| DOI | 10.1007/s00424-011-1070-y |
| Indexed | SCI(E) |
| Appears in Collections: | 第一医院 |
