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(Hypertension. 2007;49:977.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Cerebral Autoregulation and Blood Pressure Lowering

Sean Ruland; Venkatesh Aiyagari

From the Department of Neurology and Rehabilitation, University of Illinois College of Medicine, Chicago.

Correspondence to Sean Ruland, Department of Neurology and Rehabilitation, University of Illinois College of Medicine, 912 S Wood St, Room 855N (mailcode 796), Chicago, IL 60612. E-mail sruland@uic.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Despite its comparatively small size, the brain receives a disproportionate amount of blood flow compared with most other organ systems. Cerebral blood flow is closely coupled to brain metabolism and can be affected by respiratory-induced CO₂ changes and arterial blood pressure. Autoregulation is the intrinsic capacity of resistance vessels in end organs, such as heart, kidney, and brain, to dilate and constrict in response to dynamic perfusion pressure changes, maintaining blood flow relatively constant (Figure). This rapid vascular response occurs within seconds of arterial pressure fluctuations. The exact mediators of cerebral autoregulation are not completely understood. However, neurogenic stimuli; metabolic factors, such as adenosine accumulation during low perfusion; and direct intravascular pressure effects on smooth muscle or mediated via endothelial-derived relaxation factor (ie, NO) and constriction factor (ie, endothelin-1) have been implicated.¹

View larger version (9K):   Autoregulation maintains cerebral blood flow relatively constant between 50 and 150 mm Hg mean arterial pressure. The range is right shifted in chronically hypertensive patients.

The cerebral resistance vessels in normotensive individuals are known to autoregulate across a broad range of mean arterial pressures. Perfusion pressures below the lower limit result in initially increased oxygen extraction from hemoglobin and, subsequently, global ischemia. Pressures above the upper bound may result in breakthrough edema, hemorrhage, seizures, and posterior leukoencephalopathy (ie, hypertensive encephalopathy). The normal autoregulatory curve may be right shifted in chronically hypertensive patients, although the magnitude and duration over which this occurs cannot be determined on an individual basis. Hypertensive animal models have shown impaired endothelium-dependent relaxation . . . [Full Text of this Article]

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