首页> 外文期刊>Life sciences >Effect of endothelin-1 on arterial response to Bay K 8644. A comparison of ischemic and nonischemic arteries.
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Effect of endothelin-1 on arterial response to Bay K 8644. A comparison of ischemic and nonischemic arteries.

机译:内皮素-1对Bay K 8644动脉反应的影响。缺血性和非缺血性动脉的比较。

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摘要

Endothelin-1 (ET-1) has been proposed as one of the possible mediators of the vasoconstriction seen following ischemia and reperfusion. We investigated the effect of ischemia and reperfusion on the contractile response of canine renal and iliac arteries to the dihydropyridine-type calcium channel agonist (+/-)Bay K 8644, following subthreshold doses of ET-1. No significant difference in the maximum tension was observed between the ischemic and nonischemic arteries in response to Bay K 8644 in the absence of ET-1. The addition of subthreshold dose of ET-1 (10(-10) M) resulted in a significant increase in sensitivity to Bay K 8644 in both the ischemic-reperfused and non-ischemic-reperfused arteries, with a 38 fold increase in iliac arteries and about 8 fold increase in the renal arteries. However, the ET-1 potentiated response was enhanced in the ischemic-reperfused in comparison to the non-ischemic-reperfused vessels in the iliac artery. These data suggest that the potentiating mechanism of ET-1 is not only intact, but enhanced in ischemic-reperfused vessels. Since the enhanced release of ET-1 in vivo is preceded by ischemia and reperfusion, the vasospastic phenomenon observed following these events could well be mediated by ET-1.
机译:内皮素-1(ET-1)被认为是缺血和再灌注后血管收缩的可能介质之一。我们研究了亚阈值剂量的ET-1后,缺血和再灌注对犬肾和动脉对二氢吡啶型钙通道激动剂(+/-)Bay K 8644的收缩反应的影响。在没有ET-1的情况下,对Bay K 8644的缺血和非缺血动脉的最大张力之间未观察到显着差异。亚阈剂量剂量的ET-1(10(-10)M)导致缺血再灌注和非缺血再灌注动脉对Bay K 8644的敏感性显着增加,动脉增加38倍肾动脉增加约8倍。但是,与-1动脉中的非缺血再灌注血管相比,缺血再灌注中的ET-1增强反应得到增强。这些数据表明,ET-1的增强机制不仅完整,而且在缺血再灌注血管中得到增强。由于在体内缺血和再灌注之前是体内ET-1释放的增强,因此在这些事件后观察到的血管痉挛现象很可能由ET-1介导。

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