Smith Michael L, Pacchia Christina F
Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA.
Exp Physiol. 2007 Jan;92(1):45-50. doi: 10.1113/expphysiol.2006.033753. Epub 2006 Nov 10.
The link between sleep apnoea and systemic hypertension in humans is well documented. However, a direct causal association between the two diseases independent of comorbidities has been difficult to establish. Comorbidities clearly play an important role in this strong relationship; however, new findings also suggest that sleep apnoea is an independent risk factor for hypertension. This relationship appears to be at least in part a result of chronically elevated sympathetic activity, and therefore manifests as a neurally mediated hypertension. Although the mechanism(s) for this causal relationship of sleep apnoea to hypertension remains ill defined, a growing body of literature suggests that autonomic dysfunction, mediated by abnormal chemoreflex control of sympathetic activity, is a potential mechanism. Abnormal chemoreflex responses to both acute and chronic apnoea or hypoxia have been demonstrated. Hypothesized mechanisms by which chemoreflex dysfunction may contribute to chronically elevated sympathetic tone and ultimately hypertension are explored in this review. Thus, this review focuses on the current evidence linking chemoreflex function to obstructive sleep apnoea and systemic hypertension in humans and provides an analysis of these data and their implications.
睡眠呼吸暂停与人类系统性高血压之间的联系已有充分记录。然而，要确定这两种疾病之间独立于合并症的直接因果关系一直很困难。合并症显然在这种紧密关系中起着重要作用；然而，新的研究结果也表明，睡眠呼吸暂停是高血压的一个独立危险因素。这种关系似乎至少部分是由于交感神经活动长期升高所致，因此表现为神经介导的高血压。尽管睡眠呼吸暂停与高血压之间这种因果关系的机制仍不明确，但越来越多的文献表明，由交感神经活动的异常化学反射控制介导的自主神经功能障碍是一种潜在机制。对急性和慢性呼吸暂停或低氧的异常化学反射反应已得到证实。本综述探讨了化学反射功能障碍可能导致交感神经张力长期升高并最终导致高血压的假设机制。因此，本综述重点关注目前将化学反射功能与人类阻塞性睡眠呼吸暂停和系统性高血压联系起来的证据，并对这些数据及其意义进行分析。
