MODULATION OF BARORECEPTOR REFLEXES

使用直接的神经内记录(显微神经学)，我建议 扩展我对调节反射控制的因素的研究 人体的肌肉交感神经活动(MSNA)包括 精神压力、躯体传入和身体条件作用。 这项工作的独特之处包括使用显微神经照相术 研究1)MSNA对手臂和腿部的差动控制 心肺和皮肤传入和2)调制 中枢神经交感神经在反射刺激期间流出 精神压力和压力感受器的激活。我计划评估一下 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了异常反射。 人类高血压患者的控制力。 首先，有人建议进行研究，以检验这一假设是否成立 刺激动脉压力感受器之后是延长的 即使在动脉血压下降后，MSNA的抑制期也是如此 回到了控制之下。 其次，我将使用MSNA的同步录音从 来检验这一假设 心肺压力反射产生不同的控制 手臂和腿部的MSNA。 第三，我们得到了节段性的初步证据 正常人躯体传入刺激时MSNA的激活 人类。从这个概念来看，这些观察是耐人寻味的 脊椎反射通常被脊椎上抑制 机械装置。我计划从RADIUS和 腓神经来检验皮肤传入的假说 刺激(冷加压试验)产生节段性和 在完好的人类中MSNA普遍增加。 第四，我们最近证明了精神压力 增加人类腿部的MSNA。我计划测试一下 内源性阿片类药物抑制和β-肾上腺素能的假说 机制促进中枢神经交感神经的增加 在精神压力下流出。 第五，我们最近的工作表明，化学上的激活 肌肉缺血引起的敏感肌肉传入是主要的 运动时对MSNA的刺激。身体调理 最大限度地减少肌肉缺血。因此，我打算测试一下 体育锻炼会减弱MSNA的假说 对运动的反应。 MSNA的显微神经学记录是安全的，并提供了 人类反射控制研究取得实质性进展。

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.