SOCIODEMOGRAPHIC REGULATION OF CV FUNCTION AND STRUCTURE

描述：环境压力一直被认为是导致 原发性高血压的发展，特别是在非裔美国人中 (A)与高加索美国人(CA)相比，EH的患病率更高。 夸大体循环血管阻力(SVR)调节血压(BP) 对压力的反应性是环境压力通过的一条途径 被认为与EH的发展有关。环境影响评估 青年EH风险的临床前标志物只有在适当的情况下才能观察到 控制遗传影响。这可以使用双胞胎队列来实现 设计。 继续检查调查员的双胞胎健康队列(519对 CA和AA双胞胎，年龄将在14至25岁之间)，再延长五年 将为更好地了解Na+的影响提供独特的机会 保留作为增强SVR反应性和血管变化的一种机制 功能(即内皮依赖性动脉扩张；EADA)，心室 结构(即左心室质量；LVM)和24小时动态血压(ABP)。 具体目标是确定：1)环境压力有多大 与应激诱导的Na+滞留、SVR反应性和临床前相关 EH风险的标记物(即EDAD降低、静息BP、ABP和LVm增加) 这些关系在AA患者中是否比CA患者更强；2)应激是否导致 钠离子滞留是连接环境应激和临床前的一条途径 高血压风险的标志物；以及3)行为因素(即约翰·亨利主义， 愤怒的表达、社会支持、身体活动)温和的影响 环境胁迫对Na+滞留和/或SVR反应性的影响 以及EH风险的临床前标记物，特别是在AA中。 长期目标是提供对环境的更好的了解 应激对EH病理生理学的影响，这将有助于 更好地识别患EH风险增加的年轻人并在 制定改进的初级预防方案。

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.