Zholos A V, Fenech C J, Prestwich S A, Bolton T B
Department of Pharmacology and Clinical Pharmacology, St George's Hospital Medical School, London SW17 ORE, UK.
J Physiol. 2000 Nov 1;528(Pt 3):521-37. doi: 10.1111/j.1469-7793.2000.00521.x.
Using whole-cell patch-clamp recording techniques, we have examined voltage-gated ion currents in a cultured human intestinal smooth muscle cell line (HISM). Experiments were performed at room temperature on cells after passages 16 and 17. Two major components of the whole-cell current were a tetraethylammonium-sensitive (IC50 = 9 mM), iberiotoxin-resistant, delayed rectifier K+ current and a Na+ current inhibited by tetrodotoxin (IC50 A 100 nM). No measurable inward current via voltage-gated Ca2+ channels could be detected in these cells even with 10 mM Ca2+ or Ba2+ in the external solution. No current attributable to calcium-activated K+ channels was found and no cationic current in response to muscarinic receptor activation was present. In divalent cation-free external solution two additional currents were activated: an inwardly rectifying hyperpolarization-activated current, I(HA), and a depolarization-activated current, I(DA) x I(HA) and I(DA) could be carried by several monovalent cations; the sizes of currents in descending order were: K+ > Cs+ > Na+ for I(HA) and Na+ > K+ >> Cs+ for I(DA). I(HA) was activated and deactivated instantaneously and showed no inactivation whereas I(DA) was activated, inactivated and deactivated within tens of milliseconds. These currents were inhibited by external calcium with an IC50 of 0.3 microM for I(DA) and an IC50 of 20 microM for I(HA). Cyclopiazonic acid (CPA) induced an outward, but not an inward current. SK&F 96365, a blocker of store-operated Ca2+ channels, suppressed I(DA) with a half-maximal inhibitory concentration of 9 microM but was ineffective in inhibiting I(HA) at concentrations up to 100 microM. Gd3+ and La3+ strongly suppressed I(DA) at 1 and 10 microM, respectively and were less effective in blocking I(HA) (complete inhibition required a concentration of 100 microM for both). Carbachol at 10-100 microM evoked about a 3-fold increase in I(HA) amplitude and completely abolished I(DA). We conclude that I(HA) and I(DA) are Ca2+-blockable cationic currents with different ion selectivity profiles that are carried by different channels. I(DA) shows novel voltage-dependent properties for a cationic current.
利用全细胞膜片钳记录技术,我们检测了一种培养的人肠道平滑肌细胞系(HISM)中的电压门控离子电流。实验在室温下对传代16和17后的细胞进行。全细胞电流的两个主要成分是一种对四乙铵敏感(IC50 = 9 mM)、对埃博毒素不敏感的延迟整流钾电流和一种被河豚毒素抑制的钠电流(IC50约为100 nM)。即使在外部溶液中加入10 mM的Ca2+或Ba2+,在这些细胞中也检测不到可测量的通过电压门控Ca2+通道的内向电流。未发现归因于钙激活钾通道的电流,也不存在对毒蕈碱受体激活的阳离子电流。在无二价阳离子的外部溶液中,激活了另外两种电流:一种内向整流的超极化激活电流I(HA)和一种去极化激活电流I(DA)。I(HA)和I(DA)可由几种单价阳离子携带;电流大小的降序排列为:I(HA)中K+ > Cs+ > Na+,I(DA)中Na+ > K+ >> Cs+。I(HA)瞬间激活和失活,无失活现象,而I(DA)在几十毫秒内激活、失活和去激活。这些电流被外部钙抑制,I(DA)的IC50为0.3 microM,I(HA)的IC50为20 microM。环匹阿尼酸(CPA)诱导外向电流,但不诱导内向电流。SK&F 96365是一种储存操纵性Ca2+通道阻滞剂,以9 microM的半数最大抑制浓度抑制I(DA),但在浓度高达100 microM时对抑制I(HA)无效。Gd3+和La3+分别在1 microM和10 microM时强烈抑制I(DA),对I(HA)的阻断作用较小(两者完全抑制均需100 microM的浓度)。10 - 100 microM的卡巴胆碱使I(HA)幅度增加约3倍,并完全消除I(DA)。我们得出结论,I(HA)和I(DA)是具有不同离子选择性的可被Ca2+阻断的阳离子电流,由不同的通道携带。I(DA)显示出一种阳离子电流新的电压依赖性特性。