Sleep Enhancement to Decrease Blood Pressure: A Randomized, Controlled Trial

项目摘要/摘要 高血压是世界范围内心脑血管疾病的主要危险因素。这个 现在，睡眠不足的患病率不断上升，与高血压并驾齐驱。支持睡眠不足和高血压之间的因果关系的观察和实验证据尤其令人信服--每晚睡眠6小时或更少与高血压发病几率增加20%-32%相关。由于减少睡眠在很大程度上是自愿的，睡眠不足可能会得到纠正，有害的健康后果可能会逆转。然而，缺乏系统的研究和强有力的证据表明睡眠改善对健康有促进作用，也没有关于可能涉及的潜在机制的数据，特别是关于血压(BP)控制的数据。为了克服这些局限性，我们进行了一项随机对照研究，调查了8周的睡眠增强/延长对报告习惯性短睡眠(6.5小时/晚)的高血压前期和1期高血压受试者的影响。通过教育和行为干预获得的睡眠改善的降压效果将与接受健康教育的安慰剂/注意力控制条件进行比较。综合措施，包括心血管、代谢和神经内分泌标志物，辅之以分子表型和心理特征，将使人们深入了解睡眠增加与血压降低以及心血管风险总体改善之间的联系的机制和媒介。我们提出以下具体目标来比较睡眠增强/延长睡眠与安慰剂/注意控制：目的1.确定睡眠增强对24小时血压的影响。目的2.评价睡眠增强对神经循环控制和血管功能的影响。目的3.评估睡眠增加时全身和局部肾素-血管紧张素-醛固酮系统(RAAS)调节的变化。 目的4.确定睡眠增加对血压影响的代谢和神经内分泌调节因子。 这项建议建立在重要优势的基础上，包括在所调查的每个领域拥有独特经验和专业知识的跨学科调查团队、令人兴奋的初步数据，以及最大限度地减少潜在的混杂因素。在翻译框架中整合生理和分子变量，辅以心理和行为表征，将进一步支持拟议的研究。来自这些研究的数据将在制定和实施有效、低成本、促进健康的延长睡眠战略方面发挥关键作用，这些战略既适用于有针对性的，也适用于整个人口。

Project Summary/Abstract Hypertension is the major risk factor for cardiovascular and cerebrovascular diseases worldwide. The escalating prevalence of inadequate sleep now parallels that of hypertension. Observational and experimental evidence favoring a causal relation between insufficient sleep and hypertension are particularly compelling - sleeping 6 hours or less per night is associated with a 20-32% higher probability of incident hypertension. Since sleep curtailment is largely voluntary, sleep deficiency may be corrected and the detrimental health consequences potentially reversed. Nevertheless, systematic studies and robust evidence of health-promoting effects of sleep enhancement are lacking, and there are no data regarding the underlying mechanisms that may be involved, especially with regard to blood pressure (BP) control. We seek to overcome these limitations by conducting a randomized controlled study to investigate the effects of 8 weeks of sleep enhancement/extension in prehypertensive and stage 1 hypertensive subjects who report habitual short sleep (<6.5 hours/night). Antihypertensive effects of sleep enhancement achieved through education and behavioral intervention will be compared to a placebo/attention control condition receiving health education. Comprehensive measures, including cardiovascular, metabolic and neuroendocrine markers, complemented by molecular phenotyping and psychological characterization, will generate insights into the mechanisms and mediators linking enhanced sleep to any BP reduction, and to any overall improved cardiovascular risk profile. We propose the following Specific Aims comparing sleep enhancement/extension to placebo/attention control: Aim 1. To determine the impact of sleep enhancement on 24-hour BP. Aim 2. To evaluate effects of sleep enhancement on neural circulatory control and vascular function. Aim 3. To assess changes in systemic and local renin-angiotensin-aldosterone system (RAAS) regulation in response to sleep enhancement. Aim 4. To identify metabolic and neuroendocrine mediators of the effects of sleep enhancement on BP. This proposal builds upon important strengths, including an interdisciplinary team of investigators with unique experience and expertise in each of the domains investigated, exciting preliminary data, and the minimization of potential confounders. The integration of physiological and molecular variables in a translational framework, complemented by psychological and behavioral characterization, will further bolster the proposed study. Data from these studies will be pivotal in the development and implementation of effective, low cost, health promoting sleep extension strategies applicable both on a targeted and a population-wide basis.