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血管紧张素 II 受体阻滞剂可减轻年轻成年非裔美国人的应激升压反应。

Angiotensin II receptor blocker attenuates stress pressor response in young adult African Americans.

机构信息

Department of Population Health Sciences, Georgia Prevention Institute, Augusta University, Augusta, Georgia.

Department of Pediatrics, Division of Nephrology, University of Washington, Seattle, Washington.

出版信息

J Clin Hypertens (Greenwich). 2019 Aug;21(8):1191-1199. doi: 10.1111/jch.13625. Epub 2019 Jul 22.

Abstract

African Americans (AAs) are susceptible to hypertension (HTN) and its associated organ damage leading to adverse cardiovascular (CV) outcomes. Psychological stress is proposed to contribute to the development of HTN; however, the potential role of the renin-angiotensin system (RAS) in stress-related HTN in AAs is largely unknown. In this study, we tested the hypothesis that activation of RAS is a potential contributing factor for altered CV responses to stress, and suppression of angiotensin II (Ang II) activity will improve hemodynamic responses to a prolonged mental stressor in healthy young AAs. Utilizing a double-blind, randomized, crossover study design, 132 normotensive AAs (25 ± 7 years) were treated with either a placebo (PLC) or 150 mg/d irbesartan (an Ang II type 1 receptor blocker; ARB) for 1 week. On the final day of each treatment, hemodynamic measures and urinary sodium excretion (UNaV) were collected before, during and after a 45 minute-mental stress. The magnitude of stress-induced increase in blood pressure with ARB was blunted and delayed compared to PLC. Systolic blood pressure at the end of recovery on ARB was significantly lower compared to either PLC (110 ± 13 vs 117 ± 12 mm Hg respectively; P < 0.001) or the prestress level on ARB (P = 0.02). ARB treatment reduced overall vasoconstriction and improved poststress UNaV. ARB attenuated blood pressure responses to mental stress and improved the poststress BP recovery process which were partly linked to reduced overall vasoconstriction and improved stress-induced UNaV in young adult AAs prior to the development of disease conditions. These results suggest that treatment approaches that inhibit RAS action could have significant relevance to potentially lower susceptibility to stress responses and eventually the premature development of HTN in AAs.

摘要

非裔美国人(AA)易患高血压(HTN)及其相关的器官损伤,导致不良心血管(CV)结局。心理压力被认为是导致 HTN 发展的一个因素;然而,肾素-血管紧张素系统(RAS)在 AA 应激相关 HTN 中的潜在作用在很大程度上尚不清楚。在这项研究中,我们检验了 RAS 激活是导致 CV 对压力反应改变的一个潜在因素的假设,并且抑制血管紧张素 II(Ang II)的活性将改善健康年轻 AA 对长时间精神应激的血液动力学反应。采用双盲、随机、交叉研究设计,对 132 名血压正常的 AA(25 ± 7 岁)进行了为期 1 周的安慰剂(PLC)或 150mg/d 厄贝沙坦(血管紧张素 II 型 1 受体阻滞剂;ARB)治疗。在每种治疗的最后一天,在 45 分钟精神应激前、应激中和应激后收集血液动力学测量和尿钠排泄(UNaV)。与 PLC 相比,ARB 治疗时压力引起的血压升高幅度较小,延迟时间较长。与 PLC(分别为 110 ± 13 对 117 ± 12mmHg;P < 0.001)或 ARB 上的预应激水平(P = 0.02)相比,ARB 治疗后恢复期的收缩压明显降低。ARB 治疗减少了整体血管收缩,并改善了应激后 UNaV。ARB 减轻了心理应激对血压的反应,并改善了应激后的 BP 恢复过程,这在一定程度上与减少整体血管收缩和改善年轻 AA 应激后的 UNaV 有关,而这些 AA 之前没有出现疾病状态。这些结果表明,抑制 RAS 作用的治疗方法可能与降低对压力反应的易感性以及最终降低 AA 中 HTN 的过早发展具有重要相关性。

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