PHYSIOLOGICAL EFFECTS OF DIETARY SODIUM IN SALT RESISTANT HUMANS

膳食钠对耐盐人类的生理影响

• 批准号: 8359617
• 负责人: William B Farquhar
• 金额: $ 8.6万
• 依托单位: UNIVERSITY OF DELAWARE
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-03-01 至 2012-02-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8359617
• 关键词: Affect; Animals; Blood Pressure; Cardiac; Cardiology; Circadian Rhythms; Collaborations; Data; Delaware; Diet; Dietary Sodium; Discipline of Nursing; Food; Funding; Funding Mechanisms; General Population; Grant; Healthcare Systems; Hour; Human; Inbred SHR Rats; Inbred WKY Rats; Individual; Institution; Intake; Mediating; Medical Technology; National Center for Research Resources; Physiologic pulse; Physiological; Physiology; Plethysmography; Principal Investigator; Research; Research Infrastructure; Resistance; Resources; Running; Sodium; Sodium Chloride; Source; Time; Translating; United States National Institutes of Health; Universities; Urine; Venous; base; cost; dietary control; experience; graduate student; indexing; kidney vascular structure; normotensive; nutrition; pressure; salt sensitive

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Recent evidence suggests that sodium may contribute to structural and functional abnormalities, independent of blood pressure (BP). Specifically, data in experimental animals suggest that sodium-loading  independent of changes in BP  promotes cardiac, vascular, and renal damage. Deleterious physiological changes from excess sodium have been documented in spontaneously hypertensive rats, and  with particular relevance for this proposal  in normotensive Wistar-Kyoto rats. In short, there is a growing appreciation that elevated BP is not the only problem related to excess dietary sodium. The objective of this INBRE proposal is to build upon these animal studies by exploring these issues in humans; these mechanistic animal studies need to be translated to human studies. We will examine the physiological effects of dietary sodium in a group that we characterize as having salt resistant BP ( 5 mmHg change in mean BP going from a low to high sodium diet). Subjects will complete a 17-day dietary trial (3-day run-in of 100 mmol/day of sodium, 7 days high sodium (350 mmol/day) and 7 days of low sodium (20 mmol/day). All foods will be prepared for the subjects thought an established collaboration with Christiana Care Health System. Dietary compliance will be assessed by collecting 24 hours of urine on the last day of each condition; salt sensitivity of BP will be individually assessed via 24-hour ambulatory BP on the last day of each condition. Our overall hypothesis is that dietary sodium will adversely affect circadian BP rhythm, arterial function, and venous function. Circadian BP rhythm will be assessed using the night time dip in pressure; arterial function will be assessed via pulse wave velocity and augmentation index; endothelial function will be assessed via brachial flow-mediated dilation; and venous function will be assess via venous occlusion plethysmography. The strength of this proposal is the sophisticated physiological assessment that will be performed under well-controlled dietary conditions in a group that does not have "salt sensitive" BP. Habitual sodium intake is high in the general population, therefore our focus will be on demonstrating differences in these variables between the high and low sodium conditions. This proposal brings together a multi-disciplinary team which includes individuals from Physiology, Cardiology, Medical Technology, Nutrition, and Nursing. Two different institutions in the state of Delaware are involved (University of Delaware and Christiana Care Health System). This team represents a true collaborative partnership. This proposal will also provide hands-on research experience for undergraduate and graduate students. The data collected under this funding mechanism will form the basis of an R01 submission.

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 子项目的主要研究者可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 最近的证据表明，钠可能有助于结构和功能异常，独立于血压（BP）。 具体而言，实验动物的数据表明，  独立于BP的变化  促进心脏、血管和肾脏损伤。 在自发性高血压大鼠中已经记录了过量钠引起的有害生理变化，  与本提案特别相关  血压正常的Wistar-Kyoto大鼠。 简而言之，越来越多的人认识到，血压升高并不是与过量膳食钠有关的唯一问题。 本INBRE提案的目的是通过在人类中探索这些问题来建立这些动物研究;这些机制动物研究需要转化为人类研究。 我们将研究饮食钠在我们表征为具有耐盐BP（从低钠饮食到高钠饮食的平均BP变化5 mmHg）的组中的生理效应。 受试者将完成为期17天的饮食试验（3天导入期，100 mmol/天钠，7天高钠（350 mmol/天）和7天低钠（20 mmol/天））。 所有的食物都将为受试者准备，并与Christiana Care Health System建立合作关系。 将通过在每种疾病的最后一天收集24小时尿液来评估饮食依从性;将通过每种疾病的最后一天的24小时动态BP来单独评估BP的盐敏感性。 我们的总体假设是，膳食钠会对昼夜血压节律、动脉功能和静脉功能产生不利影响。 将使用夜间压力下降评估昼夜BP节律;将通过脉搏波速度和增强指数评估动脉功能;将通过肱动脉血流介导的扩张评估内皮功能;将通过静脉闭塞体积描记术评估静脉功能。 该建议的优势在于，在饮食控制良好的情况下，对没有“盐敏感”血压的人群进行复杂的生理评估。 在一般人群中，习惯性钠摄入量很高，因此我们的重点将是证明高钠和低钠条件下这些变量的差异。 该提案汇集了一个多学科团队，其中包括生理学，心脏病学，医疗技术，营养学和护理学的个人。 涉及特拉华州的两个不同机构（特拉华州大学和Christiana Care Health System）。 这是一个真正的合作伙伴关系。 该提案还将为本科生和研究生提供实践研究经验。 在这一供资机制下收集的数据将构成提交R 01的基础。