BLOOD PRESSURE CONTROL BY FOREBRAIN & BRAINSTEM NEURONS

前脑控制血压

• 批准号: 7267668
• 负责人: SUSAN M BARMAN
• 金额: $ 21.01万
• 依托单位: MICHIGAN STATE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1987
• 资助国家: 美国
• 起止时间: 1987-09-30 至 2009-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7267668
• 关键词: BLOOD; PRESSURE; CONTROL; FOREBRAIN; BRAINSTEM

DESCRIPTION (provided by applicant): The Research Plan is divided into four tightly inter-linked projects that will test novel hypotheses regarding the central neural circuitry that 1) affects basal sympathetic nerve discharge (SND) and the respiratory rhythm as reflected by phrenic nerve activity (PNA) and 2) mediates changes in SND, blood pressure (BP), and respiration produced by activation of an array of vagal and sympathetic afferents. These projects build on work completed during the current funding period and address problems from a unique perspective by focusing on the often ignored "classic pressor area" in the medullary lateral tegmental field (LTF). The experiments described in Project #1 are the first to seek to identify the source(s) of excitatory drive to LTFsympathoexcitatory neurons that help set the basal level of SND. These experiments have significant bearing on the mechanism by which the neurogenic support for resting BP is generated. Projects #2 & 3 provide the first comprehensive assessment of mechanisms by which "natural" activation of different types of visceral receptors (mechanoreceptors, chemosensitive receptors) can alter efferent SND, PNA, and ultimately cardiorespiratory function. The reflexes involve activation of myelinated and unmyelinated fibers from cardiopulmonary, gastrointestinal, and renal receptors, and responses include both excitation and inhibition of SND and/or PNA. These reflexes are thought to contribute to cardiorespiratory changes noted during physiological (e.g., lung inflation, digestion, fluid balance) as well as pathophysiological states (e.g., congestive heart failure, myocardial ischemia, sudden infant death syndrome, and esophageal dysfunction). Project #4 addresses the previously unrecognized role of the LTF in determining central respiratory rate. These studies are expected to show that medullary circuits regulating SND are more complexly organized than depicted in most current reviews and that the LTF plays a hitherto unrecognized role in regulating the respiratory rhythm.

描述（由申请人提供）：研究计划分为四个紧密相互关联的项目，这些项目将测试有关中央神经回路的新假设，即1）影响基础的交感神经排出（SND），而呼吸节奏和呼吸节奏反映，如PHRENIC神经活性（PNA）和2）介导SND，血液的交流（BP）的变化（bp），bp的激活（bp）的变化（bp），bp rance的变化（bp）的变化（bp），bp rance的变化（bp）的变化（bp）的变化。传入。这些项目建立在当前资金期间完成的工作，并通过关注髓质横向段领域（LTF）中经常被忽略的“经典压力区域”来解决问题。项目＃1中描述的实验是第一个寻求确定兴奋性驱动力来源到LTFSympathoExitation神经元的源，这些神经元有助于设定SND的基础水平。这些实验对产生静息BP的神经源支持的机制具有显着影响。项目＃2＆3提供了对机制的首次全面评估，通过这种评估，不同类型的内脏受体（机械感受器，化学敏感受体）的“自然”激活可以改变传出SND，PNA和最终心肺功能。反射涉及从心肺，胃肠道和肾脏受体激活髓鞘和无髓纤维，并且反应包括激发和抑制SND和/或PNA。这些反射被认为会导致心肺变化（例如，肺通胀，消化，液体平衡）以及病理生理态（例如，感染心脏衰竭，心肌缺血，猝死综合征和食管功能障碍）。项目＃4解决了LTF在确定中央呼吸速率中的先前未知的作用。预计这些研究将表明，调节SND的髓质回路比当前大多数评论中所描绘的更为复杂，并且LTF在调节呼吸节奏中迄今无法识别的作用。