Excessive Respiratory Modulation of Blood Pressure Triggers Hypertension
Excessive Respiratory Modulation of Blood Pressure Triggers Hypertension
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DOI：
10.1016/j.cmet.2017.01.019
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发表时间：
2017-03-07
期刊：
影响因子：
29
通讯作者：
Allen, Andrew M.
中科院分区：
文献类型：
--
作者：
Menuet, Clement;Le, Sheng;Allen, Andrew M.
高血压是世界上最大的杀手，其病因仍知之甚少，治疗方法主要针对已确定的症状，而不是病因。高血压的发展涉及交感神经活动的增加，在实验性高血压中，交感神经活动可能是由过度的呼吸调节引起的。使用选择性病毒和细胞损伤技术，我们确定延髓中的肾上腺素能 C1 神经元对于呼吸交感神经夹带和实验性高血压的发展至关重要。我们还表明，一群血压正常的年轻人，由于对运动的血压反应过度而被选择，从而增加了高血压风险，因此增强了与呼吸相关的血压波动。这些研究查明了改善高血压发展阶段过度交感神经活动的特定神经元靶标，并确定了一组将从针对这些细胞的靶标中受益的高血压前期受试者。
The etiology of hypertension, the world's biggest killer, remains poorly understood, with treatments targeting the established symptom, not the cause. The development of hypertension involves increased sympathetic nerve activity that, in experimental hypertension, may be driven by excessive respiratory modulation. Using selective viral and cell lesion techniques, we identify adrenergic C1 neurons in the medulla oblongata as critical for respiratory-sympathetic entrainment and the development of experimental hypertension. We also show that a cohort of young, normotensive humans, selected for an exaggerated blood pressure response to exercise and thus increased hypertension risk, has enhanced respiratory-related blood pressure fluctuations. These studies pinpoint a specific neuronal target for ameliorating excessive sympathetic activity during the developmental phase of hypertension and identify a group of pre-hypertensive subjects that would benefit from targeting these cells.