• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Differential vasoconstrictions induced by angiotensin II: role of AT1 and AT2 receptors in isolated C57BL/6J mouse blood vessels.
【24h】

Differential vasoconstrictions induced by angiotensin II: role of AT1 and AT2 receptors in isolated C57BL/6J mouse blood vessels.

机译：血管紧张素II诱导的差异性血管收缩：AT1和AT2受体在分离的C57BL / 6J小鼠血管中的作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Genetically altered mice are increasingly used as experimental models. However, ANG II responses in mouse blood vessels have not been well defined. Therefore, the aim of this study was to determine the role of ANG II in regulating major blood vessels in C57/BL6J mice with isometric force measurements. Our results showed that in mouse abdominal aorta ANG II induced a concentration-dependent contraction (EC50 4.6 nM) with a maximum contraction of 75.1 +/- 4.9% at 100 nM compared with that of 60 mM K+. Similarly, femoral artery also exhibited a contractile response of 76.0 +/- 3.4% to the maximum concentration of ANG II (100 nM). In contrast, ANG II (100 nM)-induced contraction was significantly less in carotid artery (24.5 +/- 6.6%) and only minimal (3.5 +/- 0.31%) in thoracic aorta. The nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester and the AT2 antagonist PD-123319 failed to enhance ANG II-induced contractions. However, an AT1 antagonist, losartan (10 microM), completely inhibitedANG II (100 nM) response in abdominal aorta and carotid artery. An AT1 agonist, [Sar1]-ANG II (100 nM), behaved similarly to ANG II (100 nM) in abdominal aorta and carotid artery. RT-PCR analyses showed that mouse thoracic aorta has a significantly lower AT1 mRNA level than abdominal aorta. These results demonstrate that major mouse vessels exhibit differential contractions to ANG II, possibly because of varied AT1 receptor levels.
机译：转基因小鼠越来越多地用作实验模型。但是，小鼠血管中的ANG II反应尚未明确。因此，本研究的目的是通过等轴测力测定确定ANG II在调节C57 / BL6J小鼠主要血管中的作用。我们的结果表明，在小鼠腹主动脉中，ANG II诱导了浓度依赖性收缩（EC50 4.6 nM），与60 mM K +相比，在100 nM时最大收缩为75.1 +/- 4.9％。同样，股动脉对ANG II（100 nM）的最大浓度也表现出76.0 +/- 3.4％的收缩反应。相比之下，ANG II（100 nM）引起的收缩在颈动脉中明显较少（24.5 +/- 6.6％），而在胸主动脉中仅有极少的收缩（3.5 +/- 0.31％）。一氧化氮合酶抑制剂Nω-硝基-L-精氨酸甲酯和AT2拮抗剂PD-123319无法增强ANG II诱导的收缩。但是，AT1拮抗剂洛沙坦（10 microM）完全抑制腹主动脉和颈动脉中的ANG II（100 nM）反应。 AT1激动剂[Sar1] -ANG II（100 nM）在腹主动脉和颈动脉中的行为类似于ANG II（100 nM）。 RT-PCR分析表明，小鼠胸主动脉的AT1 mRNA水平明显低于腹主动脉。这些结果表明，可能是由于AT1受体水平的变化，主要的小鼠血管对ANG II的收缩不同。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号