MODULATION OF BARORECEPTOR REFLEXES

使用直接神经内记录（显微神经造影术），我建议 为了扩展我对调节反射控制的因素的研究， 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造影术， 研究1）MSNA对手臂和腿部的微分控制， 心肺和皮肤传入和2）调制 在反射刺激期间的中枢神经交感神经流出， 精神压力和压力感受器激活。 我打算评估一下 这些控制机制在正常受试者，并确定是否 这些机制的改变导致异常反射 控制人类高血压。 首先，研究提出了测试的假设，持续 动脉压力感受器的刺激之后是延长的 即使在动脉压升高后，MSNA的抑制期 回到控制。 其次，我将采用MSNA的同步录音， 桡神经和腓神经，以检验假设， 心肺压力反射产生对 手臂和腿上都有。 第三，我们已经获得了分段的初步证据， 正常人躯体传入刺激时MSNA的激活 人类 这些意见是耐人寻味的概念， 脊髓反射通常被脊髓上的 机制等 我计划同时从径向和 腓神经测试假设，皮肤传入 刺激（冷加压试验）产生节段性以及 完整人体中MSNA的普遍增加。 第四，我们最近证明，精神压力 增加人类腿部的MSNA。 我打算测试一下 内源性阿片类物质抑制和β肾上腺素能 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，化学激活 肌肉缺血引起的敏感性肌肉传入是主要的 运动时对MSNA的刺激。 体能锻炼 最大限度地减少肌肉缺血。 因此，我打算测试 假设物理条件会减弱MSNA 对锻炼的反应。 MSNA的神经电图记录是安全的， 人类反射控制研究的重大进展。

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.