慢性间歇性低氧增强化学感受反射对交感活性的控制：血管紧张素 II 型 1 受体的作用。
Chronic intermittent hypoxia augments chemoreflex control of sympathetic activity: role of the angiotensin II type 1 receptor.
机构信息
Department of Kinesiology, University of Wisconsin, Madison, WI 53706, USA.
出版信息
Respir Physiol Neurobiol. 2010 Apr 15;171(1):36-45. doi: 10.1016/j.resp.2010.02.003. Epub 2010 Feb 12.
Chronic exposure to intermittent hypoxia (CIH) increases carotid sinus nerve activity in normoxia and in response to acute hypoxia. We hypothesized that CIH augments basal and chemoreflex-stimulated sympathetic outflow through an angiotensin receptor-dependent mechanism. Rats were exposed to CIH for 28 days: a subset was treated with losartan. Then, lumbar sympathetic activity was recorded under anesthesia during 20-s apneas, isocapnic hypoxia, and potassium cyanide. We measured carotid body superoxide production and expression of angiotensin II type-1 receptor, neuronal nitric oxide synthase, and NADPH oxidase. Sympathetic activity was higher in CIH vs. control rats at baseline, during apneas and isocapnic hypoxia, but not cyanide. Carotid body superoxide production and expression of angiotensin II type 1 receptor and gp91(phox) subunit of NADPH oxidase were elevated in CIH rats, whereas expression of neuronal nitric oxide synthase was reduced. None of these differences were evident in animals treated with losartan. CIH-induced augmentation of chemoreflex sensitivity occurs, at least in part, via the renin-angiotensin system.
慢性间歇性低氧（CIH）暴露会增加正常情况下和急性低氧反应时颈动脉窦神经活动。我们假设 CIH 通过血管紧张素受体依赖的机制增强基础和化学感受性刺激的交感传出。大鼠接受 CIH 暴露 28 天：其中一部分用氯沙坦治疗。然后，在麻醉下记录腰交感神经活动，在 20 秒的呼吸暂停、等二氧化碳缺氧和氰化钾期间。我们测量颈动脉体超氧化物产生和血管紧张素 II 型 1 受体、神经元型一氧化氮合酶和 NADPH 氧化酶的表达。在基础状态、呼吸暂停和等二氧化碳缺氧期间，CIH 大鼠的交感神经活动高于对照组，但氰化物除外。CIH 大鼠颈动脉体超氧化物产生和血管紧张素 II 型 1 受体和 NADPH 氧化酶的 gp91(phox)亚单位表达增加，而神经元型一氧化氮合酶的表达减少。用氯沙坦治疗的动物没有出现这些差异。CIH 诱导的化学感受性敏感性增强至少部分通过肾素-血管紧张素系统发生。
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