SODIUM & NEUROPEPTIDES IN STRESS INDUCED HYPERTENSION

应激和钠是与糖尿病发病机制有关的因素。 高血压。压力和钠这两个因素也是 与阿片类药物和血管紧张素系统相关。相当可观 有证据支持这些物质在 不同病因的高血压。然而，目前还没有 应激诱导中多种因素综合作用的研究 高血压。这项研究旨在调查 血压升高的机制(S) 压力和钠。微型脉冲多谱勒的研制 流动探测器使我们能够获得关于 清醒大鼠的血流动力学变量，到目前为止 在更大的动物身上也是可能的。作为这些技术的结果 进展现在有可能研究心血管疾病的相关性 建立应激大鼠模型。完全仪器化的意识 Wistar大鼠将被用来获得关于 血流动力学状态(血压、心输出量、总 外周阻力)以及压力感受器灵敏度 应力模型(领土应力、旋转应力和隔离 压力)，同时暴露于三种饮食钠方案(低、 正常、高钠)。再加上这个数据，某些老鼠将会 在上述实验条件下进行类似的测试，而 慢性阻断血管紧张素(沙特兰，转换酶 抑制剂)或阿片(纳洛酮)系统通过渗透微泵 输液。这些多肽的作用(如果有的话)是否 外周或中央也将使用中央或 给药技术或物质不会跨越 血脑屏障。应激与钠离子之间的相互作用 已知的与神经肽能系统的关系 将对参与心血管控制的人员进行评估。这个 防御反应，即使在警报时只被轻微激活，也是一种 对血压调节机制的主要影响。它是 很可能血管紧张素II阿片类药物的相互作用和影响 而钠盐应激是正常日常生活中的一种现象。这个 本申请中提出的研究将提供缺失的 关于这些重要相互作用的信息及其 在血压调节中的作用。阐明这些潜在的原因 机制可以提供一个基础来逆转或防止 遇到的压力和钠的有害行为 每天。

Stress and sodium are factors linked to the pathogenesis of hypertension. These two factors, stress and sodium, are also interrelated with the opiate and angiotensin systems. Substantial evidence is available supporting a role for these substances in hypertension of differing etiologies. However, there has not been a comprehensive study of these factors combined in stress induced hypertension. This study is designed to investigate the mechanism(s) responsible for elevations in blood pressure due to stress and sodium. The development of miniature pulsed Doppler flow probes has made it possible to obtain data concerning hemodynamic variables in conscious rats that until now was only possible in larger animals. As a result of these technological advances it is now possible to study cardiovascular correlates in establish rat models of stress. Fully instrumented conscious Wistar rats will be used to obtain data concerning the hemodynamic status (blood pressure, cardiac output, total peripheral resistance) as well as baroreceptor sensitivity in three models of stress (territorial stress, rotation stress and isolation stress) while being exposed to three dietary sodium regimes (low, normal, high sodium). Coupled with this data, certain rats will be similarly tested under the above experimental conditions while chronically blocking the angiotensin (sarthran, converting enzyme inhibitor) or opiate (naloxone) systems via osmotic minipump infusions. Whether the action, if any, of these peptides is peripheral or central will also be examined using either central administration techniques or substances that do not cross the blood brain barrier. Interactions between stress and sodium and the relationships with neuropeptidergic systems known to participate in cardiovascular control will be evaluated. The defense reaction, even if only slightly activated when alerted, is a major influence on blood pressure regulatory mechanisms. It is likely that interactions and influences of angiotensin II, opiates and sodium with stress is an occurrence of normal daily life. The studies proposed within this application will provide missing information concerning these important interactions and their role in blood pressure regulation. Elucidating these underlying mechanisms can provide a basis to reverse or prevent the deleterious actions of stress and sodium which are encountered daily.