Beta-adrenergic receptor mediated inflammation control by monocytes is associated with blood pressure and risk factors for cardiovascular disease.
Beta-adrenergic receptor mediated inflammation control by monocytes is associated with blood pressure and risk factors for cardiovascular disease.
复制标题
DOI：
10.1016/j.bbi.2015.08.012
复制
发表时间：
2015-11
期刊：
影响因子：
--
通讯作者：
Wilson K
中科院分区：
文献类型：
--
作者：
Hong S;Dimitrov S;Cheng T;Redwine L;Pruitt C;Mills PJ;Ziegler MG;Green JM;Shaikh F;Wilson K
压倒性的数据表明，即使是轻度高血压(BP)的个体也有很大的风险患上临床高血压和未来的心血管疾病(CVD)。对于被称为高血压前期的轻度升高的血压的治疗策略仍然缺乏共识，对其临床结果的病理生理学和机制的了解仍然有限。我们的主要目的是研究β受体介导的炎症控制(BARIC)反应与血压和心血管危险因素(包括肥胖、抑郁情绪、空腹血糖、甘油三酯和胆固醇水平)之间的关系，并与84名血压正常的人进行比较。通过测定体外Iso处理(10−8M)对内毒素刺激的单核细胞内肿瘤坏死因子产生的抑制程度来测定Baric。采用Beck抑郁量表(BDI)评定抑郁情绪。评估空腹代谢和血脂水平，并检测血浆炎症细胞因子肿瘤坏死因子、白介素1β和白介素6水平，以确认高血压前期参与者的促炎状态。与血压正常的参与者相比，高血压前期参与者年龄更大、体重更重、包括更多男性，并且表现出更高的空腹血糖、甘油三酯、胆固醇和血浆肿瘤坏死因子水平(p‘s<；0.05)。与正常血压组相比，高血压前期组的Baric显著降低(p<；0.05)。在所有参与者中，Baric与收缩压、舒张压、年龄、体重指数、空腹血糖、甘油三酯、总胆固醇和低密度胆固醇水平以及躯体抑郁症状呈负相关(p‘s<；.0001至0.05)。然而，在高血压前期个体中，即使在控制了协变量(年龄、性别、种族、BMI、血糖和血脂水平、躯体BDI评分)后，Baric仍与SBP呈正相关(p<；0.05)。两个BP组之间Baric-SBP关系的这种不同性质可能归因于缓和因素，如心肺健康或抑郁症状，而这些因素在目前的研究中无法清楚地破译。尽管如此，我们的发现表明，交感肾上腺激活介导的炎症失调与血压之间存在关联，即使在血压正常到轻度升高的个体中也可以观察到这种联系。Baric可能是一个有用和敏感的血管炎症风险升高的指标，即使在较低的血压水平也可以检测到，特别是考虑到它与传统的CVD危险因素和单核细胞在动脉粥样硬化形成过程中的关键作用。
Overwhelming data indicate that individuals with even mildly elevated blood pressure (BP) are at great risk for developing clinical hypertension and future cardiovascular disease (CVD). There remains a lack of consensus regarding treatment strategies for mildly elevated BP, termed prehypertension, and the knowledge of pathophysiology and mechanisms of its clinical outcomes remains limited. Our primary aim was to investigate βAR-mediated inflammation control (BARIC) responses of blood monocytes to isoproterenol (Iso) in relation to BP and CVD risk factors, including obesity, depressive mood, fasting glucose, triglycerides, and cholesterol levels in the 64 prehypertensive compared to 84 individuals with normal BP. BARIC was determined by measuring the degree of inhibition in lipopolysaccharides-stimulated monocytic intracellular TNF production by ex vivo Iso treatment (10−8 M). Depressive mood was assessed by Beck Depression Inventory (BDI). Fasting metabolic and lipid panels were assessed, and plasma levels of inflammatory cytokines TNF, IL-1β, IL-6 were measured in a subset to confirm proinflammatory state of prehypertensive participants. Prehypertensive participants were older, heavier, included more men, and presented higher levels of fasting glucose, triglycerides, cholesterol, and plasma TNF compared to normotensive participants (p’s< .05). BARIC was significantly attenuated in the prehypertensive compared to normotensive group (p< .05). BARIC was negatively associated with systolic BP, diastolic BP, age, BMI, fasting glucose, triglycerides, total and low density cholesterol levels, and somatic depressive symptoms in all participants (p’s< .0001 to .05). However, among the prehypertensive individuals BARIC was positively associated with SBP even after controlling for the covariates (age, gender, race, BMI, glucose and lipid panel, somatic BDI scores) (p< .05). This differing nature of the BARIC-SBP relationship between the two BP groups may be attributed to moderating factors such as cardiorespiratory fitness or depressive symptoms that could not be clearly deciphered in this current study. Nonetheless, our findings indicate the associations between inflammation dysregulation mediated by sympathoadrenal activation and BP that is observable even among individuals with normal to mildly elevated BP. BARIC may be a useful and sensitive indicator of elevated risk for vascular inflammatory disease that can be detected even at lower BP levels, especially given its associations with traditional CVD risk factors and the critical role of monocytes in atherogenic processes.