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收缩压作为肾肌源性反应的触发因素:是保护性的还是自动调节性的?

Systolic blood pressure as the trigger for the renal myogenic response: protective or autoregulatory?

作者信息

Loutzenhiser Rodger, Griffin Karen A, Bidani Anil K

机构信息

Smooth Muscle Research Group, Department of Pharmacology and Therapeutics, University of Calgary Faculty of Medicine, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N1, Canada.

出版信息

Curr Opin Nephrol Hypertens. 2006 Jan;15(1):41-9. doi: 10.1097/01.mnh.0000199011.41552.de.

DOI:10.1097/01.mnh.0000199011.41552.de
PMID:16340665
Abstract

PURPOSE OF REVIEW

The ability of the kidney to autoregulate renal blood flow and glomerular filtration rate has long been viewed as existing to prevent fluctuations in blood pressure from causing parallel fluctuations in renal function and distal delivery of filtrate. This review, however, points out that the primary consequence of the loss of this autoregulatory capacity is not a disturbance in volume regulation, but rather an increased susceptibility to hypertensive injury. Moreover, the kinetic requirements for renal protection indicate that current views of dynamic autoregulation cannot explain how the kidney is normally protected against acute elevations in systolic blood pressure.

RECENT FINDINGS

Recent findings suggest that the kinetics of the myogenic mechanism of the afferent arteriole are uniquely suited to protect against acute elevations in the systolic blood pressure, in that this vessel not only senses this rapidly oscillating blood pressure component, but that its response is exclusively dependent on this signal.

SUMMARY

These new findings are consistent with recent data indicating that it is the systolic blood pressure elevations that most closely correlate with target organ damage. The fact that the myogenic mechanism is also a necessary component of renal autoregulation may explain the strong linkage between autoregulatory impairment and increased susceptibility to hypertensive injury.

摘要

综述目的

长期以来,肾脏自动调节肾血流量和肾小球滤过率的能力被认为是为了防止血压波动导致肾功能和远端滤液输送出现平行波动。然而,本综述指出,这种自动调节能力丧失的主要后果并非是容量调节紊乱,而是对高血压损伤的易感性增加。此外,肾脏保护的动力学要求表明,目前关于动态自动调节的观点无法解释肾脏如何正常抵御收缩压急性升高。

最新发现

最近的研究结果表明,入球小动脉的肌源性机制动力学独特地适合于抵御收缩压急性升高,因为该血管不仅能感知这种快速振荡的血压成分,而且其反应完全依赖于该信号。

总结

这些新发现与最近的数据一致,这些数据表明与靶器官损伤最密切相关的是收缩压升高。肌源性机制也是肾脏自动调节的必要组成部分这一事实,可能解释了自动调节受损与高血压损伤易感性增加之间的紧密联系。

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