INWARDLY RECTIFYING POTASSIUM CURRENT IN RAT FETAL AND NEONATAL VENTRICULAR CARDIOMYOCYTES
INWARDLY RECTIFYING POTASSIUM CURRENT IN RAT FETAL AND NEONATAL VENTRICULAR CARDIOMYOCYTES
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DOI：
10.1152/ajpheart.1993.265.4.h1107
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发表时间：
1993-10-01
影响因子：
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通讯作者：
SPERELAKIS, N
中科院分区：
文献类型：
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作者：
MASUDA, H;SPERELAKIS, N
采用膜片钳技术记录新鲜分离的单胎（12天和18天）和新生儿（1、5和10天）大鼠心室肌细胞的全细胞和单通道内整流钾电流（I(K1)）。在保持电位为-40 mV的超极化测试脉冲下，整个细胞I（K1）被激发。在胎儿第12天至新生儿第5天的心脏发育过程中，I（K1）密度显著增加；在新生儿第10天没有进一步增加。用150 mM K+在移液器和液浴溶液中对单个I（K1）通道进行细胞贴附贴片记录。在胎儿第18天和新生儿第5天的细胞中均观察到具有短开口的大电导（31 pS） K+通道，但在胎儿第12天的细胞中未观察到。在胎儿第12天，大约10%的细胞中只观察到小电导（11ps）的长开口通道。新生儿第5天大导通通道打开的概率是胎儿第18天的2.6倍。综上所述，在观察到的心脏发育过程中，I（K1）密度的增加可能主要是由于I（K1）通道开放概率的增加，而不是它们数量的增加。我们认为在胎儿第12天很少观察到的小电导通道可能是一种未成熟的I（K1）通道，在发育过程中消失。
Whole cell and single-channel inwardly rectifying potassium currents (I(K1)) of freshly isolated single fetal (12 and 18 days) and neonatal (1, 5, and 10 days) rat ventricular myocytes were recorded using patch-clamp techniques. Whole cell I(K1) was elicited by hyperpolarizing test pulses from a holding potential of -40 mV. I(K1) densities increased markedly during heart development between fetal day 12 and until neonatal day 5; there was no further increase on neonatal day 10. Cell-attached patch recordings of single I(K1) channels were employed with 150 mM K+ both in the pipette and bath solutions. Large-conductance (31 pS) K+ channels with short openings were observed both in fetal day 18 and neonatal day 5 but not in fetal day 12 cells. Only small-conductance (11 pS) channels with long openings were observed in approximately 10% of the cells on fetal day 12. The open probability of the large-conductance channels was 2.6-fold greater on neonatal day 5 than on fetal day 18. In conclusion, the increase in the I(K1) density during observed heart development may be primarily due to an increase in the open probability of the I(K1) channels, rather than to an increase in their number. We suggest that the small-conductance channel infrequently observed on fetal day 12 could be an immature type of I(K1) channel, which disappears during development.