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DDT1 MF-2平滑肌细胞中P2嘌呤受体介导的膜电流

P2-purinoceptor-mediated membrane currents in DDT1 MF-2 smooth muscle cells.

作者信息

Molleman A, Nelemans A, Den Hertog A

机构信息

University of Groningen, Department of Pharmacology and Clinical Pharmacology, The Netherlands.

出版信息

Eur J Pharmacol. 1989 Oct 4;169(1):167-74. doi: 10.1016/0014-2999(89)90829-7.

Abstract

The electrophysiological response evoked by ATP was investigated in the DDT1 MF-2 smooth muscle cell line using the microelectrode technique and the whole-cell patch clamp technique. Application of ATP (10(-3) M) to the bathing solution caused a small initial depolarization of the cell membrane, followed by hyperpolarization and slow depolarization. During voltage clamping (-50 mV) a triphasic response was recorded on stimulation with ATP (10(-4)-10(-3) M). A short-lasting inward current was followed by a transient outward current and a slowly decreasing inward current. This response was not affected by the receptor antagonists, propranolol (3 X 10(-6) M), phentolamine (3 X 10(-6) M), atropine (3 X 10(-6) M) or theophylline (10(-3) M). The ATP-induced currents were not modified by the voltage-dependent channel blocking agents, tetraethyl ammonium (3 X 10(-3) M), 3,4-diaminopyridine (10(-3) M), tetrodotoxin (3 X 10(-7) M) or diltiazem (10(-5) M). The fast inward current was not detectable at a low ATP concentration (10(-5) M). The outward current showed a reversal potential near -76 mV, which equals the potassium equilibrium potential. This current was abolished after neutralization of the potassium electrochemical gradient. The outward current was suppressed under calcium-free conditions and also in the presence of tolbutamide (10(-4) M) or glipizide (5 X 10(-6) M). Guanosine triphosphate (5 X 10(-6) M) promoted the outward current, while this current was inhibited in the presence of guanosine diphosphate (5 X 10(-6) M).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

利用微电极技术和全细胞膜片钳技术,在DDT1 MF - 2平滑肌细胞系中研究了ATP诱发的电生理反应。向浴液中加入ATP(10⁻³ M)会使细胞膜先出现小的去极化,随后是超极化和缓慢去极化。在电压钳制(-50 mV)期间,用ATP(10⁻⁴ - 10⁻³ M)刺激可记录到三相反应。先是短暂的内向电流,接着是瞬时外向电流,然后是缓慢减小的内向电流。该反应不受受体拮抗剂普萘洛尔(3×10⁻⁶ M)、酚妥拉明(3×10⁻⁶ M)、阿托品(3×10⁻⁶ M)或茶碱(10⁻³ M)的影响。ATP诱导的电流也不受电压依赖性通道阻断剂四乙铵(3×10⁻³ M)、3,4 - 二氨基吡啶(10⁻³ M)、河豚毒素(3×10⁻⁷ M)或地尔硫䓬(10⁻⁵ M)的改变。在低ATP浓度(10⁻⁵ M)时检测不到快速内向电流。外向电流的反转电位接近-76 mV,这与钾离子平衡电位相等。在钾离子电化学梯度消除后,该电流消失。在无钙条件下以及存在甲苯磺丁脲(10⁻⁴ M)或格列吡嗪(5×10⁻⁶ M)时,外向电流受到抑制。三磷酸鸟苷(5×10⁻⁶ M)促进外向电流,而在二磷酸鸟苷(5×10⁻⁶ M)存在时该电流受到抑制。(摘要截断于250字)

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