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首页> 外文期刊>American Journal of Physiology >Upregulation of cardiovascular ghrelin receptor occurs in the hyperdynamic phase of sepsis.
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Upregulation of cardiovascular ghrelin receptor occurs in the hyperdynamic phase of sepsis.

机译：心血管生长激素释放肽受体的上调发生在脓毒症的高动力期。

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Ghrelin, a newly identified endogenous ligand for growth hormone secretagogue receptor 1a (GHSR-1a, i.e., ghrelin receptor), was recently demonstrated to be a potent vasoactive peptide. Although sepsis is characterized by an early, hyperdynamic phase, it remains unknown whether ghrelin or GHSR-1a plays a role in the cardiovascular response to sepsis. To determine this, polymicrobial sepsis was induced by cecal ligation and puncture in male adult rats. At 5 h (i.e., early sepsis) or 20 h (i.e., late sepsis) after cecal ligation and puncture, blood and tissue samples were collected. Ghrelin levels and ghrelin and GHSR-1a mRNA expression were assessed by RIA and RT-PCR, respectively. In addition, GHSR-1a protein levels in aorta, heart, and small intestine were determined by Western blotting. The vascular response to ghrelin was determined by using an isolated gut preparation. A primary rat aortic smooth muscle cell culture was used to determine the effects of LPS on GHSR-1a expression. The results indicate that although ghrelin levels decreased at early and late sepsis, its receptor was markedly elevated in early sepsis. Moreover, ghrelin-induced relaxation in resistance blood vessels of the isolated small intestine increased significantly during early sepsis but was not altered in late sepsis. Furthermore, GHSR-1a expression in smooth muscle cells was significantly increased at mRNA and protein levels with stimulation by LPS at 10 ng/ml. These results demonstrate that GHSR-1a expression is upregulated and vascular sensitivity to ghrelin stimulation is increased in the hyperdynamic phase of sepsis.
机译：生长激素促分泌素受体1a（GHSR-1a，即生长素释放肽受体）的新近鉴定的内源性配体生长激素释放肽最近被证明是有效的血管活性肽。尽管脓毒症的特征是早期的高动力状态，但仍不知道ghrelin或GHSR-1a是否在心血管对败血症的反应中起作用。为了确定这一点，在雄性成年大鼠中通过盲肠结扎和穿刺诱导了多菌性败血症。在盲肠结扎和穿刺后5小时（即败血症早期）或20小时（即败血症晚期），收集血液和组织样品。通过RIA和RT-PCR分别评估了Ghrelin水平以及ghrelin和GHSR-1a mRNA的表达。另外，通过Western印迹测定主动脉，心脏和小肠中的GHSR-1a蛋白水平。通过使用分离的肠制剂确定对生长激素释放肽的血管反应。使用原代大鼠主动脉平滑肌细胞培养物确定LPS对GHSR-1a表达的影响。结果表明，尽管生长激素释放肽水平在败血症的早期和晚期降低，但其受体在败血症早期显着升高。此外，生长激素释放肽诱导的分离的小肠阻力血管松弛在脓毒症早期明显增加，但在脓毒症晚期没有改变。此外，在10 ng / ml的LPS刺激下，平滑肌细胞中GHSR-1a的表达在mRNA和蛋白质水平显着增加。这些结果表明，在脓毒症的高动力期中，GHSR-1a表达上调并且对生长素释放肽刺激的血管敏感性增加。

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