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首页> 外文期刊>Brazilian Journal of Medical and Biological Research >Functional expression of kinin B1 and B2 receptors in mouse abdominal aorta
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Functional expression of kinin B1 and B2 receptors in mouse abdominal aorta

机译:激肽B1和B2受体在小鼠腹主动脉中的功能性表达

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Previous studies have shown that the vascular reactivity of the mouse aorta differs substantially from that of the rat aorta in response to several agonists such as angiotensin II, endothelin-1 and isoproterenol. However, no information is available about the agonists bradykinin (BK) and DesArg9BK (DBK). Our aim was to determine the potential expression of kinin B1 and B2 receptors in the abdominal mouse aorta isolated from C57BL/6 mice. Contraction and relaxation responses to BK and DBK were investigated using isometric recordings. The kinins were unable to induce relaxation but concentration-contraction response curves were obtained by applying increasing concentrations of the agonists BK and DBK. These effects were blocked by the antagonists Icatibant and R-715, respectively. The potency (pD2) calculated from the curves was 7.0 ± 0.1 for BK and 7.3 ± 0.2 for DBK. The efficacy was 51 ± 2% for BK and 30 ± 1% for DBK when compared to 1 μM norepinephrine. The concentration-dependent responses of BK and DBK were markedly inhibited by the arachidonic acid inhibitor indomethacin (1 μM), suggesting a mediation by the cyclooxygenase pathway. These contractile responses were not potentiated in the presence of the NOS inhibitor L-NAME (1 mM) or endothelium-denuded aorta, indicating that the NO pathway is not involved. We conclude that the mouse aorta constitutively contains B1 and B2 subtypes of kinin receptors and that stimulation with BK and DBK induces contractile effect mediated by endothelium-independent vasoconstrictor prostanoids.
机译:先前的研究表明,在响应几种激动剂(如血管紧张素II,内皮素-1和异丙肾上腺素)时,小鼠主动脉的血管反应性与大鼠主动脉的反应性有很大不同。但是,没有有关激动剂缓激肽(BK)和DesArg9BK(DBK)的信息。我们的目标是确定激肽B1和B2受体在从C57BL / 6小鼠分离的腹主动脉中的潜在表达。使用等距记录研究了对BK和DBK的收缩和松弛反应。该激肽不能诱导松弛,但是通过增加浓度的激动剂BK和DBK获得了浓度-收缩反应曲线。这些作用分别被拮抗剂依卡替班和R-715阻断。由曲线计算出的效价(pD2)对于BK为7.0±0.1,对于DBK为7.3±0.2。与1μM去甲肾上腺素相比,BK的功效为51±2%,DBK的功效为30±1%。花生四烯酸抑制剂吲哚美辛(1μM)显着抑制了BK和DBK的浓度依赖性反应,表明是由环氧合酶途径介导的。在存在NOS抑制剂L-NAME(1 mM)或内皮剥脱的主动脉的情况下,这些收缩反应未得到增强,表明NO通路不参与。我们得出的结论是,小鼠主动脉组成性地包含激肽受体的B1和B2亚型,并且用BK和DBK刺激诱导了内皮依赖性血管收缩性前列腺素介导的收缩作用。

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