CENTRAL BLOOD PRESSURE REGULATION IN AGED

老年人的中心血压调节

• 批准号: 3353976
• 负责人: RUBEN D BUNAG
• 金额: $ 8.96万
• 依托单位: UNIVERSITY OF KANSAS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 1986
• 资助国家: 美国
• 起止时间: 1986-09-30 至 1991-09-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3353976
• 关键词: aging; animal old age; artery stenosis; baroreceptors; blood pressure; cardiovascular pharmacology; denervation; disease /disorder model; electrostimulus; heart rate; hypertension; hypothalamus; kidney function; medulla oblongata; neurogenic hypertension; neurotransmitter biosynthesis; neurotransmitter metabolism; reflex; renin; sympathetic nervous system

We propose to test the hypothesis that the hypertension occurring with age results from dysfunction of brain aminergic mechanisms which normally regulate sympathetic vasomotor tone and blood pressure. Whether blood pressure also rises with age in rats, as it does in man, will first be determined by using a properly validated tail-cuff method to monitor blood pressure in different groups of aging Sprague-Dawley and Fischer 344 rats. To test for central dysfunction, cardiovascular and sympathetic nerve responses elicited by stimulating various hypothalamic and medullary centers electrically will be compared with those from younger rats of the same strain. Baroreflex sensitivity will be assessed by recording chronotropic and sympathetic nerve responses produced reflexly as blood pressure is elevated with phenylephrine or lowered with sodium nitroprusside; these baroreflex responses would then be compared with those obtained from younger normotensive or hypertensive rats. Acute and long-term effects of sinoaortic denervation (SAD) on regional hemodynamics, plasma catecholamines, and renin concentration will be measured. Brain amine synthesis and metabolism will be evaluated following renal denervation or arterial stenosis to determine whether aberrant signals from the kidneys contribute to alter central cardiovascular regulation in aged rats. If a good model for simulating the blood pressure elevation that occurs with age can be developed in rats, the model can be used to obtain information that could improve our understanding of age-related cardiovascular dysfunction and help us find ways to reduce mortality and morbidity caused by hypertension in the elderly.

我们建议检验以下假设：高血压随年龄增长而发生 脑胺能机制功能障碍的结果，通常 调节交感血管舒缩张力和血压。 是否有血 老鼠的压力也会随着年龄的增长而增加，就像人类一样，首先会 通过使用经过适当验证的尾套方法来监测血液来确定 不同组衰老 Sprague-Dawley 和 Fischer 344 大鼠的压力。 测试中枢功能障碍、心血管和交感神经 通过刺激下丘脑和延髓的各个部位而引起的反应 中心将与来自年轻大鼠的中心进行电比较 相同的菌株。 将通过记录评估压力反射敏感性 作为血液反射性产生的变时性和交感神经反应 用去氧肾上腺素升高压力或用钠降低压力 硝普钠；然后将这些压力反射反应与那些压力反射反应进行比较 从年轻的正常血压或高血压大鼠中获得。 急性和 窦主动脉去神经术（SAD）对局部血流动力学的长期影响， 将测量血浆儿茶酚胺和肾素浓度。 脑 胺的合成和代谢将在肾病后进行评估 去神经支配或动脉狭窄以确定是否存在异常信号 肾脏有助于改变老年人的中枢心血管调节 老鼠。 如果有一个很好的模型来模拟血压升高 随着年龄的增长而发生，可以在大鼠中发育，该模型可用于获得 可以提高我们对与年龄相关的理解的信息 心血管功能障碍并帮助我们找到降低死亡率和 老年人高血压引起的发病率。