MODULATION OF BARORECEPTOR REFLEXES

压力感受器反射的调节

• 批准号: 3485828
• 负责人: ALLYN L. MARK
• 金额: $ 11.39万
• 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/3485828
• 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.

我建议使用直接的内部记录（微图） 为了扩展我对调节反射控制的因素的研究 人类中的肌肉交感神经活动（MSNA） 精神压力，躯体传入和身体状况。 工作的独特功能包括使用微图像 研究1）通过 心肺和皮肤传入以及2）调节 反射刺激期间的中央神经交感神经流出（例如 精神压力和压力受体激活。 我打算评估 这些控制机制在正常受试者中，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，提出了研究以检验持续的假设 刺激动脉压力感受器之后是延伸 即使在动脉压后，MSNA的抑制期 返回控制。 第二，我将同时使用MSNA的录音 radial神经和腓神经，以检验以下假设 心肺动反射产生的差异控制 MSNA到胳膊和腿。 第三，我们获得了分段的初步证据 在正常情况下体细胞传入刺激期间的MSNA激活 人类。 考虑到概念，这些观察结果很有趣 脊柱反射通常受到上脊柱的抑制 机制。 我计划同时从radial和 腓神经来检验皮肤传入的假设 刺激（冷压测试）产生分段和 完整人类的MSNA普遍增加。 第四，我们最近证明了精神压力 增加了人类腿部的MSNA。 我打算测试 内源性阿片类药物抑制和β肾上腺素能的假设 机制有助于中央神经交感神经的增加 精神压力期间流出。 第五，我们最近的工作表明化学激活 肌肉缺血的敏感肌肉传入是主要的 运动过程中刺激MSNA。 物理条件 最小化肌肉缺血。 因此，我打算测试 假设物理条件会减弱MSNA 对运动的反应。 MSNA的微图记录是安全的，并提供了 对人类反射控制的研究的实质性进步。