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Suppression of angiotensin II stimulated responses in aortic vascular smooth muscle cells of experimental cirrhotic rats

机译:抑制实验性肝硬化大鼠主动脉血管平滑肌细胞中血管紧张素II的应答

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摘要

Functional responses to angiotensin II(AT-II) were determined in aortic vascular smooth muscle cells (VSMCs) from experimental cirrhotic rats.Our data showed that AT-II-stimulated extracellular acidification rate (ECAR),which was measured by Cytosesor microphysiometry,was significantly reduced in the aortic VSMCs from the cirrhotic rats as compared to those from the control animals.The ability of AT-II to promote formation of inositol phosphates,the second messenger produced by the activation of Gq-coupled receptors,was also considerably suppressed in the cirrhotic VSMCs.Furthermore,the maximal p42/44 MAPK phosphorylation stimulated by AT-II was significantly reduced in the cirrhotic VSMCs in contrast to that in the normal VSMCs.Taken together,our data clearly demonstrated that the functional responses to AT-II was severely suppressed in aortic VSMCs in cirrhosis,indicating the impairment of general Gq-coupled receptor signaling and subsequent biological function in the cirrhotic VSMCs.
机译:在实验性肝硬化大鼠的主动脉血管平滑肌细胞(VSMC)中测定了对血管紧张素II(AT-II)的功能反应。我们的数据表明,采用细胞传感器显微生理学测定的AT-II刺激的细胞外酸化率(ECAR)与对照组动物相比,肝硬化大鼠的主动脉VSMCs明显降低。AT-II促进肌醇磷酸酯(由Gq偶联受体活化产生的第二信使)形成的能力也被大大抑制了。此外,与正常VSMC相比,肝硬化VSMC中AT-II刺激的最大p42 / 44 MAPK磷酸化显着降低。总的来说,我们的数据清楚地表明,对AT-II的功能性反应是严重抑制肝硬化的主动脉血管平滑肌细胞,表明肝硬化性血管平滑肌细胞中一般Gq偶联受体信号转导受损和随后的生物学功能。

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