Ionic currents in single smooth muscle cells of the canine renal artery.
Ionic currents in single smooth muscle cells of the canine renal artery.
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犬肾动脉单个平滑肌细胞中的离子电流。
DOI：
10.1161/01.res.71.4.745
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发表时间：
1992
影响因子：
20.1
通讯作者：
Hume,JR
中科院分区：
文献类型：
--
作者：
Gelband,CH;Hume,JR
应用膜片钳技术记录了酶法分离的犬肾动脉平滑肌细胞全细胞和细胞贴壁两种状态下的膜电流。这些细胞的平均静息电位、输入电阻、膜时间常数和细胞电容分别为-51.8 +/- 2.1 mV、5.2 +/- 0.98 G Ω、116.2 +/- 16.4 msec和29.1 +/- 2.0 pF。内向电流，当从-80 mV的保持电位引出时，在-50 mV附近激活，在0 mV附近达到最大值，并且对二氢吡啶激动剂Bay K 8644和二氢吡啶拮抗剂尼索地平敏感。从电压阶跃和斜坡去极化中识别出两种宏观外向电流。净外向电流的主要电荷载体通过尾电流实验鉴定为K+（逆转电位，在10.8 mM [K+]或0 mM [K+]i中为-61.0 +/-0.8 mV）。第一个成分是一个小的、低噪声的、电压和时间依赖性的电流，在-40 mV和-30 mV之间激活（IK（dr）），第二个成分是一个更大的、噪声更大的、电压和时间依赖性的电流，在+10 mV的电位下激活（IK（Ca））。IK（dr）和IK（Ca）在长（4秒）电压阶跃期间几乎没有失活。用不同的Ca ~（2+）和K ~（+）通道阻断剂可使IK（Ca）和IK（dr）快速分离。IK（Ca）可被外部NiCl 2（500 μ M）、CdCl 2（300 μ M）、EGTA（5 mM）、四乙基铵（Ki为+60 mV，307 μ M）和Charybdotoxin（100 nM）显著抑制，但对4-氨基吡啶（0.1-10 mM）不敏感。IK（dr）可被4-氨基吡啶（Ki为+10 mV，723 μ M）和四乙基铵（Ki为+10 mV，908 μ M）抑制，但对外部NiCl 2（500 μ M）、CdCl 2（300 μ M）、EGTA（5 mM）和Charybdotoxin（100 nM）不敏感。两种类型的单K+通道被确定在细胞贴附补丁。记录的最丰富的K+通道表现出电压依赖性激活，被外部四乙基铵（250 μ M）阻断，并具有较大的单通道电导（在贴片移液管中，150 mM K+为232 +/- 12 pS，在贴片移液管中，5.4 mM K+为130 +/- 17 pS）。第二个通道也是电压依赖性的，被4-氨基吡啶（5 mM）阻断，并表现出较小的单通道电导（在贴片移液管中150 mM K+时为104 +/- 8 pS，在贴片移液管中5.4 mM K+时为57 +/- 6 pS）。这些结果表明，犬肾动脉细胞的去极化打开二氢吡啶敏感的Ca ~（2+）通道和至少两个K ~+通道。（400字处截断摘要）
Membrane currents from single smooth muscle cells enzymatically isolated from canine renal artery were recorded using the patch-clamp technique in the whole-cell and cell-attached configurations. These cells exhibited a mean resting potential, input resistance, membrane time constant, and cell capacitance of -51.8 +/- 2.1 mV, 5.2 +/- 0.98 G omega, 116.2 +/- 16.4 msec, and 29.1 +/- 2.0 pF, respectively. Inward current, when elicited from a holding potential of -80 mV, activated near -50 mV, reached a maximum near 0 mV and was sensitive to the dihydropyridine agonist Bay K 8644 and dihydropyridine antagonist nisoldipine. Two components of macroscopic outward current were identified from voltage-step and ramp depolarizations. The predominant charge carrier of the net outward current was identified as K+ by tail-current experiments (reversal potential, -61.0 +/- 0.8 mV in 10.8 mM [K+]o 0 mM [K+]i). The first component was a small, low-noise, voltage- and time-dependent current that activated between -40 and -30 mV (IK(dr)), and the second component was a larger, noisier, voltage- and time-dependent current that activated at potentials positive to +10 mV (IK(Ca)). Both IK(dr) and IK(Ca) displayed little inactivation during long (4-second) voltage steps. IK(Ca) and IK(dr) could be pharmacologically separated by using various Ca2+ and K+ channel blockers. IK(Ca) was substantially inhibited by external NiCl2 (500 microM), CdCl2 (300 microM), EGTA (5 mM), tetraethylammonium (Ki at +60 mV, 307 microM), and charybdotoxin (100 nM) but was insensitive to 4-aminopyridine (0.1-10 mM). IK(dr) was inhibited by 4-aminopyridine (Ki at +10 mV, 723 microM) and tetraethylammonium (Ki at +10 mV, 908 microM) but was insensitive to external NiCl2 (500 microM), CdCl2 (300 microM), EGTA (5 mM), and charybdotoxin (100 nM). Two types of single K+ channels were identified in cell-attached patches. The most abundant K+ channel that was recorded exhibited voltage-dependent activation, was blocked by external tetraethylammonium (250 microM), and had a large single-channel conductance (232 +/- 12 pS with 150 mM K+ in the patch pipette, 130 +/- 17 pS with 5.4 mM K+ in the patch pipette). The second channel was also voltage dependent, was blocked by 4-aminopyridine (5 mM), and exhibited a smaller single-channel conductance (104 +/- 8 pS with 150 mM K+ in the patch pipette, 57 +/- 6 pS with 5.4 mM K+ in the patch pipette). These results suggest that depolarization of canine renal artery cells opens dihydropyridine-sensitive Ca2+ channels and at least two K+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)
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用膜片钳方法研究平滑肌中的离子通道。
DOI：
10.2170/jjphysiol.38.1
发表时间：
1988
期刊：
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影响因子：
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作者：
T. Tomita
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影响因子：
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DOI：
10.3181/00379727-197-43234
发表时间：
1991
影响因子：
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DOI：
10.1113/jphysiol.1989.sp017641
发表时间：
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期刊：
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影响因子：
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作者：
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影响因子：
20.1
作者：
D. W. Wilde;K. Lee
通讯作者：
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