SLEEP DISORDERED BREATHING AND NEUROCIRCULATORY CONTROL

睡眠呼吸障碍（呼吸暂停、呼吸不足和上气道高 阻力）已成为高血压的独立危险因素。 这个项目的目标是确定睡眠的机制 呼吸紊乱引起急性和慢性血压升高 在人类身上。我们认为睡眠中的间歇性窒息 通过增加交感神经血管流出到血压 外周循环目的我将研究 窒息会引起持续的交感神经激活， 比化学刺激更持久我们假设缺氧， 全身性或颈动脉化学感受器，触发这种反应。 目的2将探讨交感神经系统分离的原因， 血管流出和血管阻力。 我们认为腺苷通过直接和间接的血管扩张作用， 是造成这种现象的原因。目标3和4将审查 呼吸暂停的神经循环反应机制。 我们假设 急性升压反应严重依赖于交感神经 神经系统激活，但不消除输入 肺牵张感受器目标5将确定长期- 长期经鼻持续气道加压治疗对高血压患者血压的影响 轻度至中度睡眠呼吸障碍患者。我们预计 我们的实验将解释 过度活跃和高血压见于睡眠障碍者 呼吸，反过来，导致更合理的治疗方法。

Sleep disordered breathing (apnea, hypopnea, and high upper airway resistance) has emerged as an independent risk factor for hypertension. The goal of this project is to determIne the mechanisms by which sleep disordered breathing causes acute and chronic blood pressure elevation in humans. We propose that intermittent asphyxia during sleep raises blood pressure via an increase in sympathetic vasomotor outflow to the peripheral circulation. Aim l will examine the mechanisms by which exposure to asphyxia causes persistent sympathetic activation which outlasts the chemical stimuli. We hypothesize that hypoxia, acting systemically or at the carotid chemoreceptor, triggers this response. Aim 2 will investigate the cause of dissociation between sympathetic vasomotor outflow and vascular resistance during exposure to asphyxia. We propose that adenosine, via direct and indirect vasodilator effects, is responsible for this phenomenon. Aims 3 and 4 will examine mechanisms for neurocirculatory responses to apnea. We hypothesize that the acute pressor response is critically dependent on sympathetic nervous system activation but not on elimination of input from pulmonary stretch receptors. Aim 5 will determine the effects of long- term nasal continuous airway pressure treatment on blood pressure in individuals with mild to moderate sleep disordered breathing. We expect that our experiments will provide explanations for the sympathetic overactivity and hypertension seen in individuals with sleep disordered breathing and, in turn, lead to a more rational approach to therapy.