MODULATION OF BARORECEPTOR REFLEXES

压力感受器反射的调节

• 批准号: 3485825
• 负责人: ALLYN L. MARK
• 金额: $ 14.57万
• 依托单位: UNIVERSITY OF IOWA
• 依托单位国家: 美国
• 财政年份: 1979
• 资助国家: 美国
• 起止时间: 1979-12-01 至 1992-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3485825
• 关键词: afferent nerve; angiography; baroreceptors; beta antiadrenergic agent; cardiovascular pharmacology; exercise; heart rate; human subject; hypertension; hypotension; opiate alkaloid; plethysmography; spinal reflex; stress; sympathetic nervous system; vascular resistance

Using direct intraneural recordings (microneurography), I propose to extend my research on factors that modulate reflex control of muscle sympathetic nerve activity (MSNA) in humans including mental stress, somatic afferents and physical conditioning. Unique features of the work include use of microneurography to study 1) differential control of MSNA to arm and leg by cardiopulmonary and cutaneous afferents and 2) modulation of central neural sympathetic outflow during reflex stimuli such as mental stress and baroreceptor activation. I plan to evaluate these control mechanisms in normal subjects and to determine if alterations in these mechanisms contribute to abnormal reflex control in human hypertensives. First, studies are proposed to test the hypothesis that sustained stimulation of arterial baroreceptors is followed by an extended period of inhibition of MSNA even after arterial pressure has returned to control. Second, I will employ simultaneous recordings of MSNA from radial and peroneal nerves to test the hypothesis that cardiopulmonary baroreflexes produce differential control of MSNA to arm and leg. Third, we have obtained preliminary evidence for segmental activation of MSNA during somatic afferent stimulation in normal humans. These observations are intriguing in view of the concept that spinal reflexes are normally inhibited by supraspinal mechanisms. I plan simultaneous recordings from radial and peroneal nerves to test the hypothesis that cutaneous afferent stimulation (cold pressor test) produces segmental as well as generalized increases in MSNA in intact humans. Fourth, we have recently demonstrated that mental stress increases MSNA in the leg in humans. I plan to test the hypothesis that endogenous opioids inhibit and beta adrenergic mechanisms facilitate increases in central neural sympathetic outflow during mental stress. Fifth, our recent work suggests that activation of chemically sensitive muscle afferents by muscle ischemia is the principal stimulus to MSNA during exercise. Physical conditioning minimizes muscle ischemia. I therefore intend to test the hypothesis that physical conditioning will attenuate MSNA responses to exercise. Microneurographic recordings of MSNA are safe and provide a substantial advance for studies of reflex control in humans.

我建议使用直接神经内记录（显微神经造影） 扩展我对调节反射控制的因素的研究 人类的肌肉交感神经活动（MSNA）包括 精神压力、躯体传入和身体调节。 这项工作的独特之处包括使用显微神经描记术 研究 1) MSNA 对手臂和腿部的差异控制 心肺和皮肤传入神经和 2) 的调节 反射刺激期间中枢神经交感神经流出，例如 精神压力和压力感受器激活。 我打算评估一下 正常受试者中的这些控制机制并确定是否 这些机制的改变导致反射异常 控制人类高血压。 首先，提出研究来检验持续存在的假设 刺激动脉压力感受器后，会延长 即使在动脉压降低后，MSNA 仍处于抑制期 恢复了控制。 其次，我将使用 MSNA 的同步记录 桡神经和腓神经来检验以下假设： 心肺压力反射产生不同的控制 MSNA 到手臂和腿。 第三，我们已经获得了分部的初步证据。 正常体细胞传入刺激过程中 MSNA 的激活 人类。 鉴于这个概念，这些观察结果很有趣 脊髓反射通常受到脊髓上神经的抑制 机制。 我计划从径向和 腓神经来检验皮肤传入神经的假设 刺激（冷加压试验）产生节段以及 完整人类中 MSNA 普遍增加。 第四，我们最近证明精神压力 增加人类腿部的 MSNA。 我计划测试 假设内源性阿片类药物抑制和β肾上腺素能 机制促进中枢神经交感神经的增加 精神压力时流出。 第五，我们最近的工作表明化学活化 肌肉缺血引起的敏感肌传入是主要的 运动期间 MSNA 的刺激。 身体调理 最大限度地减少肌肉缺血。 因此我打算测试 假设身体调节会减弱 MSNA 对运动的反应。 MSNA 的显微神经影像记录是安全的，并提供 人类反射控制研究取得了重大进展。