电场刺激释放的内源性三磷酸腺苷（ATP）通过大鼠离体尾动脉中的P2x和P2y嘌呤受体引起收缩。
Endogenous ATP released by electrical field stimulation causes contraction via P2x- and P2y-purinoceptors in the isolated tail artery of rats.
作者信息
Fukumitsu A, Takano Y, Iki A, Honda K, Saito R, Katsuragi T, Kamiya H
机构信息
Department of Pharmacology, Faculty of Pharmaceutical Sciences, School of Medicine, Fukuoka University, Japan.
出版信息
Jpn J Pharmacol. 1999 Dec;81(4):375-80. doi: 10.1254/jjp.81.375.
Electrical field stimulation (EFS) caused contraction of isolated tail arteries of rats. The EFS-induced contraction showed frequency-dependence and was entirely abolished by the sodium channel blocker tetrodotoxin (1 x 10(-7) M). The EFS-induced (at 20 Hz) contraction was reduced by about 60% in the presence of phentolamine (1 x 10(-6) M). Therefore, later experiments were carried out in the presence of phentolamine. Pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) (1 x 10(-8)-1 x 10(-6) M) and basilen blue E-3G (3 x 10(-5)-5 x 10(-5) M), P2-receptor antagonists, significantly inhibited the contraction evoked by EFS. In addition, PPADS significantly inhibited the contractions induced by ATP (1 x 10(-4) M) and a selective P2x-receptor agonist, alpha,beta-methylene ATP (1 x 10(-6) M). In contrast, basilen blue E-3G did not inhibit alpha,beta-methylene ATP-induced contraction. The ecto-ATPase activator apyrase (5 and 10 U/ml) significantly reduced the EFS-induced contractions. These findings suggest that endogenous ATP released by EFS causes contractions of rat tail artery via both the P2x-receptors and P2y-receptors.
电场刺激（EFS）可引起大鼠离体尾动脉收缩。EFS诱导的收缩呈现频率依赖性，且完全被钠通道阻滞剂河豚毒素（1×10⁻⁷ M）所阻断。在酚妥拉明（1×10⁻⁶ M）存在的情况下，EFS诱导的（20 Hz时）收缩减少了约60%。因此，后续实验在酚妥拉明存在的条件下进行。P2受体拮抗剂磷酸吡哆醛 - 6 - 偶氮苯 - 2',4'-二磺酸（PPADS）（1×10⁻⁸ - 1×10⁻⁶ M）和碱性蓝E - 3G（3×10⁻⁵ - 5×10⁻⁵ M）显著抑制了EFS诱发的收缩。此外，PPADS显著抑制了由ATP（1×10⁻⁴ M）和选择性P2x受体激动剂α,β - 亚甲基ATP（1×10⁻⁶ M）诱导的收缩。相比之下，碱性蓝E - 3G并不抑制α,β - 亚甲基ATP诱导的收缩。胞外ATP酶激活剂腺苷三磷酸双磷酸酶（5和10 U/ml）显著降低了EFS诱导的收缩。这些发现表明，EFS释放的内源性ATP通过P2x受体和P2y受体引起大鼠尾动脉收缩。
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