How an increase in blood pressure, in and of itself, induces hypertensive nephrosclerosis is unclear. In an earlier study we found that leukocyte infiltration, proximal tubular cell proliferation, matrix deposition and interstitial fibrosis occur in the unclipped kidney of 2 K 1 C Goldblatt hypertensive rats. In this study we tested the hypothesis that the cell surface adhesion molecule ICAM-1 is expressed on the vascular endothelium and tubular epithelium of unclipped kidneys at 4 weeks. As a positive control, we examined the clipped kidney as well. We found that systolic blood pressure was significantly elevated in renovascular hypertensive rats compared to sham-operated controls after 4 weeks (198 +/- 5 mmHg vs 121 +/- 2 mmHg, P < 0.001). Furthermore, quantitative (densitometry) measurements showed that ICAM-1 expression on vascular endothelium and on tubular cells was significantly increased in unclipped kidneys compared to controls (P < 0.05). The same was true for monocyte and granulocyte infiltration (P < 0.05). These same variables were even more prominent in the clipped kidneys, compared to unclipped and control kidneys (P < 0.05). Our data show that ICAM-1 is expressed in unclipped kidneys exposed to hypertension as well as in clipped kidneys exposed to ischemia. We suggest that mechanical injury induced by increased blood pressure is responsible for an inflammatory adhesion molecule-mediated response and concomitant renal injury.

译文

目前尚不清楚血压本身的升高如何引起高血压肾硬化。在较早的研究中,我们发现2 K 1 C Goldblatt高血压大鼠的未夹肾中发生白细胞浸润,近端肾小管细胞增殖,基质沉积和间质纤维化。在这项研究中,我们测试了以下假设: 细胞表面粘附分子ICAM-1在4周时在未夹住的肾脏的血管内皮和肾小管上皮上表达。作为阳性对照,我们也检查了截断的肾脏。我们发现,与假手术对照组相比,肾血管性高血压大鼠的收缩压在4周后显着升高 (198/- 5 mmHg vs 121/- 2 mmHg,P <0.001)。此外,定量 (密度测定法) 测量显示,与对照组相比,未夹住的肾脏在血管内皮和肾小管细胞上的ICAM-1表达显着增加 (P <0.05)。单核细胞和粒细胞浸润也是如此 (P <0.05)。与未夹肾和对照肾相比,这些相同的变量在夹肾中更为突出 (P <0.05)。我们的数据显示,ICAM-1在暴露于高血压的未夹肾以及暴露于缺血的夹肾中表达。我们建议由血压升高引起的机械损伤是炎症粘附分子介导的反应和伴随的肾损伤的原因。

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