BRADYKININ‐INDUCED RELAXATION OF RENAL AND PULMONARY ARTERIES IS DEPENDENT UPON INTACT ENDOTHELIAL CELLS
BRADYKININ‐INDUCED RELAXATION OF RENAL AND PULMONARY ARTERIES IS DEPENDENT UPON INTACT ENDOTHELIAL CELLS
复制标题
缓激肽诱导的肾动脉和肺动脉松弛依赖于完整的内皮细胞
DOI：
10.1111/j.1476-5381.1981.tb09948.x
复制
发表时间：
1981
影响因子：
7.3
通讯作者：
N. Chand
中科院分区：
文献类型：
--
作者：
B. Altura;N. Chand
当哺乳动物和人类的大部分动脉被切除时，体外对激动素的反应，特别是螺旋切割的血管条，通常是一种收缩反应；通常没有观察到任何反应。这与激肽的原位血管扩张作用形成鲜明对比。这一转变的原因(S)尚不清楚。体外实验表明，在保持内皮完整的前提下，缓激肽对去甲肾上腺素收缩的犬离体肺内动脉(阈值浓度为7.5±2.7×10−10M)和肾动脉(阈值浓度=3.2±1.6×10−10M)均有较强的松弛作用。选择性的机械破坏血管内皮细胞将缓激肽的血管扩张活性转变为收缩或根本没有反应。我们的结果可能解释了为什么之前的研究人员发现，缓激肽通常会导致切除的外周动脉收缩，而不是松弛。
When most arteries are removed from mammals and man, the in vitro response to kinins, particularly of helically‐cut vascular strips, is usually one of contraction; and often no response is observed. This is in sharp contrast to the in situ arterial vasodilator action of kinins. The reason(s) for this transformation is not known. The present in vitro experiments demonstrate that bradykinin can produce potent relaxation of canine isolated intrapulmonary arteries (threshold concentration = 7.5±2.7×10−10m) and renal arteries (threshold concentration = 3.2 ± 1.6 × 10−10m) contracted by phenylephrine, provided the endothelium is left intact. Selective, mechanical destruction of the endothelium transforms the vasodilator activity of bradykinin to either contraction or to no response at all. Our results probably explain why previous investigators have found that bradykinin usually induced contraction, rather than relaxation, of excised peripheral arteries.