SODIUM SENSITIVITY AND BLOOD PRESSURE RESPONSE

钠敏感性和血压反应

基本信息

批准号：
3351446
负责人：
GORDON H WILLIAMS
金额：
$ 48.16万
依托单位：
BRIGHAM AND WOMEN'S HOSPITAL
依托单位国家：
美国
项目类别：
财政年份：
1985
资助国家：
美国
起止时间：
1985-09-30 至 1990-03-31
项目状态：
已结题

项目摘要

Evidence favoring a role for sodium intake in the pathogenesis of hypertension has arisen from multiple sources. However, it is also clear that therapeutic approaches based on modification of sodium intake or the use of diuretic therapy are only effective in some patients. Our working hypothesis is that sodium-sensitive hypertension is not a homogeneous group, but includes patients with some forms of secondary hypertension (primary aldosteronism bilateral renal artery stenosis, and chronic renal failure), low-renin essential hypertension, and some patients with normal and high-renin essential hypertension. This proposal addresses four specific questions: First, does the blood pressure increment with sodium loading and blood pressure decrement wih diuretic therapy identify the same patient with "salt-sensitive hypertension"? These are the two major criteria for salt sensitivity. Secondly, is there a more simple and precise screening test for salt-sensitive hypertension? Specifically, we plan to assess the level of a number of potentially salt-sensitive biologic indices in normal and hypertensive subjects, including: the ouabain-like inhibitor of sodium/potassium ATPase, a factor which modifies in vitro vascular reactivity, intracellular sodium and/or calcium content and sodium transport in the red cell, platelet angiotensin II (AII) receptor number, and in vivo vascular (particularly renovascular) and adrenal responsiveness to AII. Thirdly, we will examine the effect of changes in dietary sodium intake (sodium dose-response curve) on the above mentioned indices in normal subjects to determine whether there is a hierachical utilization of these various factors as sodium intake changes; is the activation of each an off-on phenomenon of dose related? Finally, we will determine whether the relationship between the level of sodium intake and any of these biologic variables is different between hypertensives versus normal subjects, old versus young, white versus non-white, and whether salt-sensitive hypertensives have a different pattern than salt-insensitive hypertensives. Successful completion of these studies will provide a more rational and practical basis for identifying patients in whom specific recommendations for therapy can be made, provide insight into the mechanism(s) by which sodium intake induces hypertension in some patients, and delineate the underlying abnormalities in these patients.

支持钠摄入在糖尿病发病机制中发挥作用的证据高血压有多种来源。不过，也明确的是基于改变钠摄入量或使用利尿剂治疗仅对部分患者有效。我们的工作假设钠敏感性高血压不是同质的组，但包括患有某些形式的继发性高血压的患者（原发性醛固酮增多症、双侧肾动脉狭窄、慢性肾动脉狭窄衰竭），低肾素原发性高血压，以及一些正常的患者和高肾素原发性高血压。该提案涉及四个具体问题：一、钠会导致血压升高吗利尿治疗的负荷和血压下降具有相同的意义 “盐敏感性高血压”患者？这是两个主要的盐敏感性标准。其次，有没有更简单的盐敏感性高血压的精准筛查试验？具体来说，我们计划评估一些潜在的盐敏感生物制品的水平正常和高血压受试者的指数，包括：哇巴因样钠/钾 ATP 酶抑制剂，一种体外修饰因子血管反应性、细胞内钠和/或钙含量以及钠红细胞中的转运、血小板血管紧张素 II (AII) 受体数量、以及体内血管（特别是肾血管）和肾上腺反应性到所有。第三，我们将检查膳食钠变化的影响摄入量（钠剂量反应曲线）对上述指标的影响正常受试者以确定是否存在分层利用这些各种因素随着钠摄入量的变化而变化；是每个的激活关断现象与剂量有关吗？最后，我们将确定是否钠摄入量与这些因素之间的关系高血压患者与正常人之间的生物变量不同受试者，老年人与年轻人，白人与非白人，以及是否盐敏感型高血压与盐不敏感型高血压的模式不同高血压。成功完成这些研究将提供更多识别特定患者的合理和实用的基础可以提出治疗建议，深入了解钠摄入在某些患者中诱发高血压的机制，并描述这些患者潜在的异常情况。

项目成果

期刊论文数量（7）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Blunted renal vascular response to angiotensin II is associated with a common variant of the angiotensinogen gene and obesity.

肾血管对血管紧张素 II 的反应减弱与血管紧张素原基因的常见变异和肥胖有关。

DOI：
发表时间：
1996-02
期刊：
影响因子：
4.9
作者：
Hopkins, P N;Lifton, R P;Hollenberg, N K;Jeunemaitre, X;Hallouin, M C;Skuppin, J;Williams, C S;Dluhy, R G;Lalouel, J M;Williams, R R;Williams, G H
通讯作者：
Williams, G H

Hypertension, dyslipidemia, and insulin resistance: links in a chain or spokes on a wheel?

高血压、血脂异常和胰岛素抵抗：链条上的环节还是轮子上的辐条？

DOI：
发表时间：
1996-08
期刊：
影响因子：
4.4
作者：
Hopkins, P N;Hunt, S C;Wu, L L;Williams, G H;Williams, R R
通讯作者：
Williams, R R

Non-modulation as an intermediate phenotype in essential hypertension.

非调节作为原发性高血压的中间表型。

DOI：
发表时间：
1992-12
期刊：
影响因子：
0
作者：
Williams, G H;Dluhy, R G;Lifton, R P;Moore, T J;Gleason, R;Williams, R;Hunt, S C;Hopkins, P N;Hollenberg, N K
通讯作者：
Hollenberg, N K

Angiotensin-mediated renin suppression is altered in non-modulating hypertension.

血管紧张素介导的肾素抑制在非调节性高血压中发生改变。