Sanborn W G, Langer G A
J Gen Physiol. 1970 Aug;56(2):191-217. doi: 10.1085/jgp.56.2.191.
Arterially cannulated rabbit interventricular septal tissue was exposed to 5-40 microM La in 2.5 mM Ca perfusate. Immediately following perfusion with La two concurrent events were consistently observed: (a) a rapid decline of active tension to a lesser steady-state value, and (b) an abrupt, release of short duration of tissue-bound Ca. The magnitude of both events was directly related to the La. If the duration of exposure to La was brief, contractility returned toward normal upon return to the La-free perfusate. Elevation of Ca during exposure to La counteracted its effect and induced a concurrent displacement of tissue-bound La. Cellular action potentials recorded during brief perfusion with La demonstrated that essentially normal regenerative depolarization was maintained. Analysis of the quantities of (45)Ca released following exposure to 10 microM La indicated that this La-susceptible Ca was being displaced from a homogeneous pool-the one previously shown by Langer to represent contractile dependent Ca. These data led to the following conclusions: During perfusion with 2.5 mM Ca contractile dependent Ca was derived primarily from "superficially" located sites. La effected the release of contractile dependent Ca by modifying the normal permselectivity of this "superficial" membrane for activator Ca. These and other data infer that contractile dependent Ca is derived primarily from superficially located sites.
将动脉插管的兔室间隔组织暴露于含2.5 mM钙的灌注液中5 - 40 microM的镧。在用镧灌注后,立即持续观察到两个同时发生的事件:(a) 主动张力迅速下降至较低的稳态值,以及 (b) 组织结合钙的短暂突然释放。这两个事件的程度都与 La 直接相关。如果暴露于镧的时间短暂,回到无镧灌注液后收缩性会恢复正常。在暴露于镧期间升高 Ca 可抵消其作用并导致组织结合镧的同时移位。在用镧短暂灌注期间记录的细胞动作电位表明基本维持了正常的再生性去极化。对暴露于10 microM镧后释放的 (45)Ca 量的分析表明,这种对镧敏感的钙正从一个均匀池中被置换出来——之前兰格证明该池代表收缩依赖性钙。这些数据得出以下结论:在灌注2.5 mM钙期间,收缩依赖性钙主要来自“表面”位置的位点。镧通过改变这种“表面”膜对激活钙的正常通透选择性来影响收缩依赖性钙的释放。这些以及其他数据推断收缩依赖性钙主要来自表面位置的位点。