课题基金 / 基金详情

SOCIODEMOGRAPHIC REGULATION OF CV FUNCTION AND STRUCTURE

SOCIODEMOGRAPHIC REGULATION OF CV FUNCTION AND STRUCTURE
CV功能和结构的社会人口调节
批准号:
6613059
负责人:
Frank A Treiber
金额:
$0.83万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1996
资助国家:
美国
项目状态:
已结题
起止时间:
1996-09-01 至 2004-11-30

项目摘要

项目成果

Frank A Treiber的其他基金

相关文献

中文摘要
翻译
描述:环境压力已被假设为有助于 原发性高血压(EH)的发展,特别是在非洲裔美国人中 (AAs)与高加索美国人(CA)相比,他们的EH患病率更高。 全身血管阻力(SVR)介导的血压(BP)升高 对压力的反应是环境压力 被认为与EH的发展有关。环境影响评估 对青年EH风险的临床前标志物的影响, 控制基因的影响。这可以通过使用双胞胎队列来实现 设计 继续检查研究者的双胞胎CV健康队列(519对 CA和AA双胞胎谁将是14至25岁)的额外五年 将为更好地了解Na+的影响提供独特的机会, 保留作为一种机制,增加SVR的反应性和血管的变化, 函数(即,内皮依赖性动脉扩张 结构(即,左心室质量(LVM)和24小时动态血压(ABP)。 具体目的是确定:1)环境压力在多大程度上是 与应激诱导的Na+潴留、SVR反应性和临床前 EH风险的标志物(即,EDAD降低,静息BP、ABP和LVM升高) AA中的这些关系是否比CA更强; 2)压力是否会诱发 Na+潴留是连接环境应激与临床前 EH风险的标志物;和3)行为因素(即约翰·亨利主义, 愤怒的表达,社会支持,体育活动)的中度影响 环境胁迫对胁迫诱导的Na+潴留和/或SVR响应性的影响 以及EH风险的临床前标志物,特别是AA。 长期目标是更好地了解环境 压力对EH病理生理学的影响,这将有助于 更好地识别高血压风险增加的青年, 制定改进的初级预防方案。
英文摘要
DESCRIPTION: Environmental stress has been hypothesized as contributing to the development of essential hypertension (EH), particularly in African Americans (AAs) who have a higher prevalence of EH compared to Caucasian Americans (CAs). Exaggerated systemic vascular resistance (SVR) mediated blood pressure (BP) responsivity to stress is one pathway through which environmental stress is thought to be linked to development of EH. Assessment of environmental effects on preclinical markers of EH risk in youth can be observed only with proper control for genetic influences. This can be accomplished using a twin cohort design. Continued examination of the investigator's Twin CV Health cohort (519 pairs of CA and AA twins who will be 14 to 25 years old) for an additional five years will provide the unique opportunity to better understand the effects of Na+ retention as a mechanism augmenting SVR responsivity and changes in vascular function (i.e., endothelium dependent arterial dilation; EDAD), ventricular structure (i.e., left ventricular mass; LVM) and 24-hour ambulatory BP (ABP). The specific aims are to determine: 1) To what extent is environmental stress related to stress induced Na+ retention, SVR responsivity and preclinical markers of EH risk (i.e., decreased EDAD, increased resting BP, ABP, and LVM) and are these relationships stronger in AAs than CAs; 2) Whether stress induced Na+ retention is a pathway linking environmental stress with preclinical markers of EH risk; and 3) Whether behavioral factors (i.e. John Henryism, anger expression, social support, physical activity) moderate effects of environmental stress on stress induced Na+ retention and/or SVR responsivity and in the preclinical markers of EH risk, particularly in AAs. The long-term objectives are to provide a better understanding of environmental stress-related influences on the pathophysiology of EH, which will assist in better identification of youth at increased risk for EH and aid in the development of improved primary prevention programs.
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