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首页> 外文期刊>American Journal of Physiology >Adult rat cardiomyocytes exhibit capacitative calcium entry.
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Adult rat cardiomyocytes exhibit capacitative calcium entry.

机译：成年大鼠心肌细胞表现出电容性钙进入。

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摘要

Capacitative Ca(2+) entry (CCE) refers to the influx of Ca(2+) through plasma membrane channels activated on depletion of endoplasmic-sarcoplasmic reticulum Ca(2+) stores. We utilized two Ca(2+)-sensitive dyes (one monitoring cytoplasmic free Ca(2+) and the other free Ca(2+) within the sarcoplasmic reticulum) to determine whether adult rat ventricular myocytes exhibit CCE. Treatments with inhibitors of the sarcoplasmic endoplasmic reticulum Ca(2+)-ATPases were not efficient in releasing Ca(2+) from stores. However, when these inhibitors were coupled with either Ca(2+) ionophores or angiotensin II (an agonist generating inositol 1,4,5 trisphosphate), depletion of stores was observed. This depletion was accompanied by a significant influx of extracellular Ca(2+) characteristic of CCE. CCE was also observed when stores were depleted with caffeine. This influx of Ca(2+) was sensitive to four inhibitors of CCE (glucosamine, lanthanum, gadolinium, and SKF-96365) but not to inhibitors of L-type channels or the Na(+)/Ca(2+) exchanger. In the whole cell configuration, an inward current of approximately 0.7 pA/pF at -90 mV was activated when a Ca(2+) chelator or inositol (1,4,5)-trisphosphate was included in the pipette or when Ca(2+) stores were depleted with a Ca(2+)-ATPase inhibitor and ionophore. The current was maximal at hyperpolarizing voltages and inwardly rectified. The channel was relatively permeant to Ca(2+) and Ba(2+) but only poorly to Mg(2+) or Mn(2+). Taken together, these data support the existence of CCE in adult cardiomyocytes, a finding with likely implications to physiological responses to phospholipase C-generating agonists.
机译：电容性Ca（2+）条目（CCE）是指通过质膜通道流入Ca（2+）的内质-肌浆网Ca（2+）存储耗尽而激活。我们利用两种Ca（2+）敏感染料（一种监测胞质网中的胞质游离Ca（2+）和另一种游离Ca（2+））来确定成年大鼠心室肌细胞是否表现出CCE。肌浆内质网Ca（2 +）-ATPases抑制剂的治疗不能有效地从存储中释放Ca（2+）。但是，当这些抑制剂与Ca（2+）离子载体或血管紧张素II（产生肌醇1,4,5三磷酸酯的激动剂）偶联时，会观察到存储耗尽。这种消耗伴随着大量的CCE特征的细胞外Ca（2+）涌入。当商店中的咖啡因耗尽时，也会观察到CCE。 Ca（2+）的涌入对CCE的四种抑制剂（葡萄糖胺，镧，g和SKF-96365）敏感，但对L型通道或Na（+）/ Ca（2+）交换子的抑制剂不敏感。在整个电池配置中，当移液管中包含Ca（2+）螯合剂或肌醇（1,4,5）-三磷酸酯或Ca（2）时，在-90 mV时激活了大约0.7 pA / pF的内向电流。 +）的存储被耗尽的Ca（2 +）-ATPase抑制剂和离子载体。在超极化电压下电流最大，并向内整流。该通道相对渗透到Ca（2+）和Ba（2+），但几乎不渗透到Mg（2+）或Mn（2+）。综上所述，这些数据支持成人心肌细胞中CCE的存在，这一发现可能与对产生磷脂酶C的激动剂的生理反应有关。

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