SODIUM & NEUROPEPTIDES IN STRESS INDUCED HYPERTENSION

应激和钠是与糖尿病发病机制相关的因素， 高血压 这两个因素，压力和钠， 与阿片和血管紧张素系统相关。 实质性 有证据支持这些物质在以下方面的作用 不同病因的高血压。 然而， 综合研究这些因素结合在应激诱导 高血压 本研究旨在调查 导致血压升高的机制 压力和钠。 小型脉冲多普勒的研制 流量探头使得获得有关 到目前为止， 在大型动物中也是可能的。 由于这些技术 现在可以研究心血管相关性， 建立大鼠应激模型。 完全仪器化意识 将使用Wistar大鼠获得关于 血流动力学状态（血压、心输出量、总 外周阻力）以及压力感受器敏感性在三个 应力模型（区域应力、旋转应力和隔离 应激）同时暴露于三种膳食钠方案（低， 正常，高钠）。 再加上这些数据，某些老鼠将 在上述实验条件下进行类似的测试， 慢性阻断血管紧张素（sarthran，转化酶 抑制剂）或阿片（纳洛酮）系统 输液 这些肽的作用，如果有的话， 还将使用中央或中央 给药技术或物质，不跨越 血脑屏障 压力和钠之间的相互作用， 与神经肽能系统的关系， 将对参与心血管控制进行评价。 的 防御反应，即使只有轻微激活时，警报，是一个 对血压调节机制的重要影响。 是 血管紧张素II、阿片类药物 钠与压力是正常的日常生活中发生的事情。 的 本申请中提出的研究将提供缺失的 关于这些重要的相互作用及其 调节血压的作用。 阐明这些潜在的 机制可以提供一个基础，扭转或防止 遇到的应力和钠的有害作用 日报

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.