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Blood pressure and TNF-α act synergistically to increase leucocyte CD11b adhesion molecule expression in the BELFAST study: implications for better blood pressure control in ageing

机译:血压和TNF-α协同作用以增加BELFAST研究中的白细胞CD11b粘附分子表达:改善衰老过程中的血压控制意义

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摘要

Hypertension, a key risk factor for stroke, cardiovascular disease and dementia, is associated with chronic vascular inflammation, and although poorly understood, putative mechanisms include pro-inflammatory responses induced by mechanical stretching, with cytokine release and associated up-regulated expression of adhesion molecules. Because blood pressure increases with age, we measured baseline and tumour necrosis alpha (TNF-α)-stimulated CD11b/CD18 adhesion molecule expression on leucocytes to assess any association between the two. In 38 subjects (mean age 85 years), consecutively enrolled from Belfast Elderly Longitudinal Free-Living Aging Study (BELFAST), baseline and TNF-α-stimulated CD11b/CD18 expression on separated monocytes and neutrophils increased with systolic blood pressure >120 mmHg (p = 0.05) and for lymphocytes, with diastolic blood pressure >80 mmHg (p < 0.05).These findings show increased potential stickiness of intravascular cells with increasing blood pressure which is accentuated by TNF-α, and suggest mechanistic reasons why better hypertension control is important.
机译:高血压是中风,心血管疾病和痴呆症的关键危险因素,与慢性血管发炎有关,尽管人们对其了解甚少,但推测的机制包括机械拉伸引起的促炎反应,细胞因子释放以及相关的黏附分子表达上调。由于血压随年龄增长而增加,因此我们测量了基线和肿瘤坏死α(TNF-α)刺激的白细胞CD11b / CD18粘附分子表达,以评估两者之间的任何关联。在38位受试者(平均年龄85岁)中,连续从贝尔法斯特老年人纵向自由活动研究(BELFAST)入选,基线和TNF-α刺激的CD11b / CD18在分离的单核细胞和中性粒细胞中的表达随收缩压> 120毫米汞柱而升高( p = 0.05)和舒张压> 80 mmHg(p <0.05)的淋巴细胞。这些发现显示,随着TNF-α的升高,血压升高,血管内细胞的潜在黏性增加,并提出了更好控制高血压的机制原因很重要

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