SODIUM SENSITIVITY OF HYPERTENSION AND AGING

高血压和衰老的钠敏感性

• 批准号: 6097845
• 负责人: NORMAN K HOLLENBERG
• 金额: --
• 依托单位: MASSACHUSETTS GENERAL HOSPITAL
• 依托单位国家: 美国
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-06-01 至 1999-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6097845
• 关键词: ACE inhibitors; aging; aldosterone; angiotensin /renin /aldosterone hypertension; angiotensin II; atrial natriuretic peptide; blood chemistry; blood pressure; catecholamines; creatinine; dietary potassium; dietary sodium; glomerular filtration rate; human old age (65+); human subject; kidney circulation; kidney function; nutrition related tag; posture; renin; salt intake; urinalysis; young adult human (21-34)

A predictable loss of renal perfusion, glomerular filtration rate and many of the kidneys' functions -- including the ability to handle sodium -- occurs with increasing age. Hypertension, which is sensitive to sodium intake, also increases in frequency with increasing age. This study is designed to explore the responsible mechanisms for the limited ability of the aging kidney to handle salt, and its relation to the hypertension. Our first hypothesis is that a functional element contributes to the loss of renal perfusion and to the limitation of sodium handling with increasing age. Our second hypothesis is that the intrarenal generation of AII, prompted by afferent arteriolar organic lesions or an increasing frequency of glomerular obsolescence, contributes to a number of the abnormal features of aging including renal vasoconstriction, limited sodium handling, renin suppression, and a limited natriuretic response to atrial natriuretic peptide. Our third hypothesis, based on the first two, is that angiotensin converting enzyme inhibition will increase renal perfusion, restore more normal sodium handling, restore the kidneys' response to atrial natriuretic peptide and prevent the hypertension. Central to our approach is the application of proven methods to provide a rigorous assessment of steady state sodium balance and to assess the determinants of sodium balance in humans. Successful completion of these protocols will provide insight into the pathogenesis of many of the features of aging and a more rational approach to prevention and treatment.

可预见的肾脏灌注，肾小球滤过率和许多 肾功能的功能 - 包括处理钠的能力 - 随着年龄的增长而发生。 高血压，对钠敏感 摄入量，随着年龄的增长，频率也会增加。 这项研究是 旨在探讨负责机制的有限能力 老化的肾脏处理盐，及其与高血压的关系。 我们的 第一个假设是功能元素有助于丧失 肾脏灌注和钠处理的限制 年龄。 我们的第二个假设是AII的内部产生， 由传入的小动脉有机病变或频率越来越多 肾小球过时的，有助于许多异常 衰老的特征，包括肾血管收缩，有限的钠 处理，肾素抑制以及对房屋的纳地尿作用有限的反应 亚钠肽。 我们基于前两个的第三个假设是 血管紧张素转化酶抑制会增加肾脏灌注， 恢复更正常的钠处理，恢复肾脏对 心房尿液肽并防止高血压。 我们的中心 方法是实现的方法来提供严格的 评估稳态钠平衡并评估的决定因素 人类的钠平衡。 这些协议的成功完成将 洞悉衰老的许多特征的发病机理 一种更合理的预防和治疗方法。