Neural Control of Blood Pressure in Chronic Intermittent Hypoxia.
Neural Control of Blood Pressure in Chronic Intermittent Hypoxia.
复制标题
慢性间歇性缺氧血压的神经控制。
DOI：
10.1007/s11906-016-0627-8
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发表时间：
2016-03
影响因子：
5.6
通讯作者：
Cunningham, J. Thomas
中科院分区：
文献类型：
--
作者：
Shell, Brent;Faulk, Katelynn;Cunningham, J. Thomas
睡眠呼吸暂停（SA）的患病率正在增加，通常与高血压共病。慢性间歇性缺氧被用来模拟SA中观察到的动脉低氧血症，通过这种模式，SA诱导的高血压的机制正在变得清晰。睡眠期间的周期性低氧暴露长期刺激颈动脉化学反射，诱导感觉长期易化，并驱动交感神经从后脑流出。升高的交感神经紧张驱动高血压和肾交感神经活动至肾脏，导致血浆肾素活性增加，并最终外周血管紧张素II（Ang II）增加。在清醒时，当呼吸正常化时，交感神经活动不会减少。这部分是因为适应导致控制交感神经流出的后脑区域过度激活，如孤束核（NTS）和延髓头端腹外侧（RVLM）。持续的交感神经活动也是由于前脑通过室旁核（PVN）的突触信号增强。在清醒的时间，当化学感受器不暴露于缺氧时，前脑室周器官（CVO）被来自升高的血浆肾素活性的外周循环Ang II刺激。由于Ang II信号传导，CVO和正中视前核长期激活PVN。总之，这导致夜间平均动脉压（MAP）升高作为对低氧血症的反应，以及不适当地升高昼夜MAP作为对适应不良的反应。
Sleep apnea (SA) is increasing in prevalence and is commonly comorbid with hypertension. Chronic intermittent hypoxia is used to model the arterial hypoxemia seen in SA, and through this paradigm, the mechanisms that underlie SA-induced hypertension are becoming clear. Cyclic hypoxic exposure during sleep chronically stimulates the carotid chemoreflexes, inducing sensory long-term facilitation, and drives sympathetic outflow from the hindbrain. The elevated sympathetic tone drives hypertension and renal sympathetic activity to the kidneys resulting in increased plasma renin activity and eventually angiotensin II (Ang II) peripherally. Upon waking, when respiration is normalized, the sympathetic activity does not diminish. This is partially because of adaptations leading to overactivation of the hindbrain regions controlling sympathetic outflow such as the nucleus tractus solitarius (NTS), and rostral ventrolateral medulla (RVLM). The sustained sympathetic activity is also due to enhanced synaptic signaling from the forebrain through the paraventricular nucleus (PVN). During the waking hours, when the chemoreceptors are not exposed to hypoxia, the forebrain circumventricular organs (CVOs) are stimulated by peripherally circulating Ang II from the elevated plasma renin activity. The CVOs and median preoptic nucleus chronically activate the PVN due to the Ang II signaling. All together, this leads to elevated nocturnal mean arterial pressure (MAP) as a response to hypoxemia, as well as inappropriately elevated diurnal MAP in response to maladaptations.
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DOI：
10.1523/jneurosci.3367-10.2010
发表时间：
2010-09-08
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Coleman CG;Wang G;Park L;Anrather J;Delagrammatikas GJ;Chan J;Zhou J;Iadecola C;Pickel VM
通讯作者：
Pickel VM
影响因子：
3.3
作者：
Cutler, MJ;Swift, NM;Smith, ML
通讯作者：
Smith, ML
DOI：
10.1152/ajpheart.00358.2007
发表时间：
2007-11-01
影响因子：
4.8
作者：
Gu, He;Lin, Min;Cheng, Zixi Jack
通讯作者：
Cheng, Zixi Jack
影响因子：
2.9
作者：
Costa, Kaue M.;Moraes, Davi J. A.;Machado, Benedito H.
通讯作者：
Machado, Benedito H.
DOI：
10.1161/hypertensionaha.112.193789
发表时间：
2012-07
期刊：
Hypertension (Dallas, Tex. : 1979)
影响因子：
--
作者：
Cunningham JT;Knight WD;Mifflin SW;Nestler EJ
通讯作者：
Nestler EJ