内皮源性松弛因子对p2y -嘌呤受体诱导的离体大鼠肾脏血管舒张的作用

Rosemary Wangensteen, Oscar Fernández, Juan Sainz, Andrés Quesada, Félix Vargas, Antonio Osuna
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引用次数: 10

摘要

我们研究了内皮源性松弛因子一氧化氮(NO)、内皮源性超极化因子(EDHF)和前列腺素(pg)对P2Y1-和p2y2嘌呤受体诱导的离体大鼠肾脏血管舒张的作用。为此,我们分析了正常情况下大鼠肾脏血管对ATP、2-甲基硫代ATP和UTP的反应,以及同时给予nw -硝基-l-精氨酸(l-NAME)、增加K+浓度、吲哚美辛、l-NAME和增加K+后的肾脏反应。我们的结果表明,在大鼠离体灌注肾中,EDHF和NO对P2Y1-和p2y2嘌呤受体激活的血管扩张反应起作用。
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Contribution of endothelium-derived relaxing factors to P2Y-purinoceptor-induced vasodilation in the isolated rat kidney

We examined the role of endothelium-derived relaxing factors nitric oxide (NO), endothelium-derived hyperpolarising factor (EDHF), and prostaglandins (PGs) to P2Y1- and P2Y2-purinoceptor-induced vasodilation in isolated rat kidney. To do it, we analysed the renal response to ATP, 2-methylthio ATP, and UTP in rat renal vasculature under normal conditions and after the administration of: Nw-nitro-l-arginine (l-NAME), increased K+ concentration, indomethacin, and l-NAME and increased K+ together. Our results indicate that the vasodilator response to P2Y1- and P2Y2-purinoceptor activation in the isolated perfused kidney of rats is subserved by EDHF and NO.

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