Action of niflumic acid on evoked and spontaneous calcium‐activated chloride and potassium currents in smooth muscle cells from rabbit portal vein
Action of niflumic acid on evoked and spontaneous calcium‐activated chloride and potassium currents in smooth muscle cells from rabbit portal vein
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尼氟酸对家兔门静脉平滑肌细胞诱发和自发钙激活氯电流和钾电流的作用
DOI：
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发表时间：
1994
影响因子：
7.3
通讯作者：
W. Large
中科院分区：
文献类型：
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作者：
R. Hogg;Q. Wang;W. Large
1研究了尼氟灭酸对兔离体门静脉细胞自发性和诱发性钙激活氯（ICl（Ca））和钾（IK（Ca））电流的作用。2在含钾溶液中，采用制霉菌素穿孔贴片技术，在- 77 mV的保持电位（钾平衡电位）下，尼氟灭酸对自发瞬时内向电流（STIC，钙激活氯电流）幅度产生浓度依赖性抑制。使STIC振幅降低50%的浓度（IC 50）为3.6 × 10−6 m。3在-77 mV的保持电位下，尼氟灭酸使STIC衰减由单一指数衰减变为两个指数衰减。在尼氟灭酸的快速组件的衰减速度更快，和缓慢的组件是慢于控制衰减时间常数。增加尼氟灭酸的浓度增强了快组分的衰减速率，降低了慢组分的衰减速率。4尼氟灭酸对STIC振幅的影响具有电压依赖性，在-50 mV和+50 mV时，IC 50值分别为2.3 × 10−6 m和1.1 × 10−6 m（参见3.6？10−6 m（−77 mV）。5在- 50 mV和+ 50 mV电位下的无钾溶液中，尼氟灭酸没有诱导双指数STIC衰减，但只是以浓度依赖性方式增加了两种电位下的衰减时间常数。6浓度高达5 × 10−5 M的硝氟灭酸对自发性钙激活钾电流没有影响。7尼氟灭酸抑制去甲肾上腺素和咖啡因诱发的ICl（Ca），IC 50为6.6 × 10−6 m，即与自发电流相比，对诱发电流的抑制效力较低。相反，尼氟灭酸（2 × 10−6 m-5 × 10−5 m）增加去甲肾上腺素和咖啡因诱导的IK（Ca）。8讨论了尼氟灭酸阻断ICl（Ca）的机制及其作为评估ICl（Ca）在生理机制中作用的药理学工具的适用性。
1 The action of niflumic acid was studied on spontaneous and evoked calcium‐activated chloride (ICl(Ca)) and potassium (IK(Ca)) currents in rabbit isolated portal vein cells. 2 With the nystatin perforated patch technique in potassium‐containing solutions at a holding potential of – 77 mV (the potassium equilibrium potential), niflumic acid produced a concentration‐dependent inhibition of spontaneous transient inward current (STIC, calcium‐activated chloride current) amplitude. The concentration to reduce the STIC amplitude by 50% (IC50) was 3.6 × 10−6 m. 3 At – 77 mV holding potential, niflumic acid converted the STIC decay from a single exponential to 2 exponential components. In niflumic acid the fast component of decay was faster, and the slow component was slower than the control decay time constant. Increasing the concentration of niflumic acid enhanced the decay rate of the fast component and reduced the decay rate of the slow component. 4 The effect of niflumic acid on STIC amplitude was voltage‐dependent and at – 50 and + 50 mV the IC50 values were 2.3 × 10−6 m and 1.1 × 10−6 m respectively (cf. 3.6 × 10−6 m at −77 mV). 5 In K‐free solutions at potentials of – 50 mV and + 50 mV, niflumic acid did not induce a dual exponential STIC decay but just increased the decay time constant at both potentials in a concentration‐dependent manner. 6 Niflumic acid, in concentrations up to 5 × 10−5 m, had no effect on spontaneous calcium‐activated potassium currents. 7 Niflumic acid inhibited noradrenaline‐ and caffeine‐evoked ICl(Ca) with an IC50 of 6.6 × 10−6 m, i.e. was less potent against evoked currents compared to spontaneous currents. In contrast niflumic acid (2 × 10−6 m–5 × 10−5 m) increased noradrenaline‐ and caffeine‐induced IK(Ca). 8 The results are discussed with respect to the mechanism of block of ICl(Ca) by niflumic acid and its suitability as a pharmacological tool for assessing the role of ICl(Ca) in physiological mechanisms.
影响因子：
3.6
作者：
M. M. White-M.;M. Aylwin
通讯作者：
M. M. White-M.;M. Aylwin