Na+/Ca2+ exchange and cell contraction in isolated neonatal and adult rabbit cardiac myocytes.
Na+/Ca2+ exchange and cell contraction in isolated neonatal and adult rabbit cardiac myocytes.
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分离的新生和成年兔心肌细胞中的 Na /Ca2 交换和细胞收缩。
DOI：
10.1152/ajpheart.1995.268.4.h1723
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Klitzner,TS
中科院分区：
文献类型：
--
作者：
Wetzel,GT;Chen,F;Klitzner,TS
最近的研究表明，未成熟心肌中电压门控 Ca2+ 电流 (ICa) 相对缺乏。我们假设，发育中的心脏收缩部分是由于 Ca2+ 通过“反向”Na+/Ca2+ 交换电流 (INa/Ca) 流入所致。因此，在单个新生儿和成年兔心室肌细胞中测量了 INa/Ca 和细胞收缩幅度。 INa/Ca 取决于 Ca2+ 浓度、Na+ 浓度和膜电位，可被 5 mM Ni2+ 阻断，但不会被 Ca(2+) 通道阻断剂硝苯地平阻断。在新生儿细胞中，收缩幅度达到去极化正向 0 mV 的平台。在成体肌细胞中，收缩幅度在 0 mV 时最大，在正膜电位时下降。用硝苯地平抑制ICa不影响新生儿肌细胞的最大收缩幅度，但几乎完全抑制成体细胞的收缩。这些数据表明，新生兔心肌细胞的收缩不需要通过 ICa 流入 Ca2+。此外，通过逆转Na+/Ca2+交换机制的Ca2+流入可能提供Ca2+调节细胞收缩的重要部分，特别是在去极化至正膜电位期间。
Recent studies have demonstrated a relative deficiency in voltage-gated Ca2+ currents (ICa) in immature myocardium. We hypothesized that contraction in developing heart results in part from Ca2+ influx via “reverse” Na+/Ca2+ exchange current (INa/Ca). Accordingly, INa/Ca and cell contraction amplitude were measured in single neonatal and adult rabbit ventricular myocytes. INa/Ca was dependent on Ca2+ concentration, Na+ concentration, and membrane potential and was blocked by 5 mM Ni2+ but not by the Ca(2+)-channel blocker nifedipine. In neonatal cells, contraction amplitude reached a plateau for depolarizations positive to 0 mV. In adult myocytes, contraction amplitude was maximal at 0 mV and decreased at positive membrane potentials. Inhibition of ICa with nifedipine did not affect maximal contraction amplitude in neonatal myocytes but almost completely suppressed contraction of adult cells. These data suggest that Ca2+ influx via ICa is not required for contraction of neonatal rabbit cardiac myocytes. Moreover, Ca2+ influx via reversal of the Na+/Ca2+ exchange mechanism may provide a significant portion of the Ca2+ regulating cell contraction, especially during depolarization to positive membrane potentials.