Wasserman A J, McClellan G, Somlyo A P
Circ Res. 1986 Jun;58(6):790-802. doi: 10.1161/01.res.58.6.790.
Electron probe x-ray microanalysis of the composition of rabbit portal anterior mesenteric vein smooth muscle was performed following sodium loading and washout into sodium-free lithium solutions. Sodium and lithium were also measured with atomic absorption spectrophotometry. Cellular uptake of sodium and loss of potassium during sodium loading were much faster at high (37 degrees C) than at low (2 degrees C) temperature, as was the passive ouabain-resistant uptake of potassium during lithium washout. The loss of sodium at 2 degrees C into lithium solution consisted of two components: a rapid efflux that was complete by 30 minutes, and a slow component that required at least 24 hours for completion. The amount of sodium lost through the first component (approximately 200-300 mmol/kg dry weight) was relatively independent of the amount of sodium loading. The loss of cellular sodium at 2 degrees C, after 30 minutes, was accompanied by a gain of cellular lithium. Ouabain-resistant sodium loss and lithium and potassium uptake were markedly accelerated at 37 degrees C; sodium loss was complete (1200 mmol sodium/kg dry weight lost) by 30 minutes of washout. Sodium-loaded cells also lost chloride ion and gained magnesium during sodium efflux at 37 degrees C. Mitochondrial and nuclear sodium and potassium were correlated with the respective cytoplasmic concentrations during both sodium loading and sodium washout, indicating the relatively rapid equilibration of the monovalent ions between the cytoplasm and organelles. Calcium-free solutions markedly inhibited the ouabain-resistant sodium and chloride ion effluxes and potassium influx in muscles incubated, after sodium loading, in lithium solutions at 37 degrees C. These fluxes could be restored to near normal values by 0.2 mM calcium. The calcium sensitivity of the ouabain-resistant sodium, potassium, and chloride ion fluxes observed in this and other studies raises the possibility that some abnormalities of monovalent ion transport observed in cells of hypertensives are secondary to changes in cellular calcium.
在将钠加载并冲洗到无钠锂溶液后，对兔门静脉前肠系膜静脉平滑肌的成分进行了电子探针X射线微分析。钠和锂也用原子吸收分光光度法进行了测量。在钠加载过程中，细胞对钠的摄取和钾的丢失在高温（37摄氏度）下比在低温（2摄氏度）下快得多，锂冲洗过程中钾的被动哇巴因抗性摄取也是如此。在2摄氏度下，钠进入锂溶液的丢失由两个部分组成：一个快速外流，在30分钟内完成，一个缓慢部分，至少需要24小时完成。通过第一部分丢失的钠量（约200 - 300 mmol/kg干重）相对独立于钠加载量。在2摄氏度下，30分钟后细胞钠的丢失伴随着细胞锂的增加。在37摄氏度时，哇巴因抗性钠丢失以及锂和钾摄取明显加速；冲洗30分钟后钠丢失完成（丢失1200 mmol钠/kg干重）。在37摄氏度的钠外流过程中，加载钠的细胞还丢失了氯离子并获得了镁。在钠加载和钠冲洗过程中，线粒体和细胞核中的钠和钾与各自的细胞质浓度相关，表明单价离子在细胞质和细胞器之间相对快速地达到平衡。无钙溶液显著抑制了在37摄氏度下加载钠后在锂溶液中孵育的肌肉中哇巴因抗性钠和氯离子外流以及钾内流。通过0.2 mM钙可将这些通量恢复到接近正常值。在本研究和其他研究中观察到的哇巴因抗性钠、钾和氯离子通量的钙敏感性增加了这样一种可能性，即高血压患者细胞中观察到的一些单价离子转运异常是细胞钙变化的继发结果。
