Stretch-activated ion channels in tissue-cultured chick heart.
Stretch-activated ion channels in tissue-cultured chick heart.
复制标题
DOI：
10.1152/ajpheart.1993.264.3.h960
复制
发表时间：
1993-03
期刊：
影响因子：
--
通讯作者：
A. Ruknudin;Frederick Sachs;J. Bustamante
中科院分区：
文献类型：
--
作者：
A. Ruknudin;Frederick Sachs;J. Bustamante
采用单通道膜片钳技术，在组织培养的鸡胚心肌细胞上发现了五种不同类型的牵张激活离子通道。在移液器中加入140 mM K+盐水时，4个通道的线性电导约等于25、50、100和200 pS，另一个通道为内向整流器，在0 mV膜电位下约等于25 pS。100-和200-pS通道是K+选择性的，而其他通道通过碱金属阳离子和Ca 2+。从反转电位可以看出，非选择性通道的K ~+/Na ~+通透性比值（PK/PNa）为3-7，而K（+）选择性通道的K ~+/Na ~+通透性比值（PK/PNa）为7-16。对于线性电导，通道密度约等于0.3/微米2，对于内向整流器，通道密度约等于0.1/微米2。开放通道噪声是移液管填充溶液的函数，均方根（RMS）噪声以K+ <等渗蔗糖（加痕量离子）< Na+的顺序增加，可能反映了细胞外离子的短暂阻断。所有通道均被20 μ M Gd 3+阻断。25 pS线性通道也被12.5 μ M河豚毒素和10 μ M地尔硫卓阻断，但其他在这些浓度下不敏感。细胞外Cs+和氯化四乙铵没有阻断任何通道。我们在没有胚胎提取物（EE）的情况下生长的细胞中没有看到SAC活性，这表明通道表达或一些必要的辅因子在生长因子的控制下。碱性成纤维细胞生长因子（FGF）可以取代EE支持通道表达。能够产生内向电流的SAC的存在可能解释了拉伸如何增加心脏的自律性。由于某些SAC对Ca 2+具有渗透性，它们可能有助于Starling曲线，并可能启动牵张诱导的肥大。
With use of single-channel patch-clamp recording, we found five distinct types of stretch-activated ion channels (SACs) in tissue-cultured embryonic chick cardiac myocytes. With 140 mM K+ saline in the pipette, four channels had linear conductances of approximately equal to 25, 50, 100, and 200 pS and other channel was an inward rectifier of approximately equal to 25 pS at 0 mV membrane potential. The 100- and 200-pS channels were K+ selective, whereas the others passed alkali cations and Ca2+. From reversal potentials, the permeability ratio of K+/Na+, PK/PNa, was 3-7 for nonselective channels and 7-16 for K(+)-selective channels. Channel density was approximately equal to 0.3/microns2 for linear conductances and approximately equal to 0.1/microns2 for inward rectifier. Open-channel noise was a function of pipette filling solution with root-mean-square (RMS) noise increasing in the order K+ < isosmotic sucrose (plus trace ions) < Na+, probably reflecting short-lived block by extracellular ions. All channels were blocked by 20 microM Gd3+. The 25-pS linear channel was also blocked by 12.5 microM tetrodotoxin and 10 microM diltiazem, but the others were insensitive at these concentrations. Extracellular Cs+ and tetraethylammonium chloride did not block any channels. We saw no SAC activity in cells grown without embryo extract (EE), which demonstrates that channel expression, or some necessary cofactor, is under control of growth factors. Basic fibroblast growth factor (FGF) could replace EE in supporting channel expression. The presence of SACs capable of generating inward currents might explain how stretch increases automaticity in the heart. Because some SACs were permeable to Ca2+, they could contribute to the Starling curve and perhaps to initiating stretch-induced hypertrophy.