Sympathoadrenal mechanisms in the pathogenesis of sleep apnea-related hypertension
Sympathoadrenal mechanisms in the pathogenesis of sleep apnea-related hypertension
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DOI：
10.1007/s11906-009-0037-2
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发表时间：
2009-06-01
影响因子：
5.6
通讯作者：
Logan, Alexander G.
中科院分区：
文献类型：
--
作者：
Friedman, Oded;Logan, Alexander G.
阻塞性睡眠呼吸暂停低通气（OSAH）被认为是持续高血压的一个越来越常见的原因。绝大多数将这些实体联系起来的机制研究都集中在交感神经激活的作用上。因此，本综述通过强调过去5年进行的研究来解决这一据称的机制，这些研究涉及与osah相关的交感神经调节变化，独立于肥胖，以及可能与这些变化相关的干预因素和途径。最后，重点讨论了持续气道正压（CPAP）治疗引起的交感神经调节变化的研究。综上所述，这些发现加强了交感肾上腺压力系统对OSAH患者高血压状态发展至关重要的说法。
Obstructive sleep apnea-hypopnea (OSAH) is regarded as an increasingly common cause of sustained hypertension. The vast majority of mechanistic studies linking these entities have focused on the role of sympathoactivation. This review therefore addresses this purported mechanism by highlighting studies conducted in the past 5 years that speak to OSAH-related changes in sympathoregulation, independent of obesity, as well as the intervening players and pathways that may be relevant to such changes. Finally, studies with a focus on changes in sympathoregulation induced by continuous positive airway pressure (CPAP) therapy are discussed. Taken together, these findings strengthen the claim that the sympathoadrenal pressor system is essential for the development of the hypertensive state in individuals with OSAH.