Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels

Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels Abstract Faraci, Frank M., and Donald D. Heistad. Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels. Physiol. Rev. 78: 53–97, 1998. — Several new concepts have emerged in relation to mechanisms that contribute to regulation of the cerebral circulation. This review focuses on some physiological mechanisms of cerebral vasodilatation and alteration of these mechanisms by disease states. One mechanism involves release of vasoactive factors by the endothelium that affect underlying vascular muscle. These factors include endothelium-derived relaxing factor (nitric oxide), prostacyclin, and endothelium-derived hyperpolarizing factor(s). The normal vasodilator influence of endothelium is impaired by some disease states. Under pathophysiological conditions, endothelium may produce potent contracting factors such as endothelin. Another major mechanism of regulation of cerebral vascular tone relates to potassium channels. Activation of potassium channels appears to mediate relaxation of cerebral vessels to diverse stimuli including receptor-mediated agonists, intracellular second messengers, and hypoxia. Endothelial- and potassium channel-based mechanisms are related because several endothelium-derived factors produce relaxation by activation of potassium channels. The influence of potassium channels may be altered by disease states including chronic hypertension, subarachnoid hemorrhage, and diabetes. Footnotes Original studies by the authors that are summarized in this review were supported by National Institutes of Health Grants NS-24621, HL-38901, AG-10269, HL-16066, and HL-14355 and American Heart Association Grant-in-Aid 95014510. F. M. Faraci is an Established Investigator of the American Heart Association. Copyright © 1998 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Physiological Reviews The American Physiological Society

Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels

Physiological Reviews, Volume 78 (1): 53 – Jan 1, 1998

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The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0031-9333
eISSN
1522-1210
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Abstract

Abstract Faraci, Frank M., and Donald D. Heistad. Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels. Physiol. Rev. 78: 53–97, 1998. — Several new concepts have emerged in relation to mechanisms that contribute to regulation of the cerebral circulation. This review focuses on some physiological mechanisms of cerebral vasodilatation and alteration of these mechanisms by disease states. One mechanism involves release of vasoactive factors by the endothelium that affect underlying vascular muscle. These factors include endothelium-derived relaxing factor (nitric oxide), prostacyclin, and endothelium-derived hyperpolarizing factor(s). The normal vasodilator influence of endothelium is impaired by some disease states. Under pathophysiological conditions, endothelium may produce potent contracting factors such as endothelin. Another major mechanism of regulation of cerebral vascular tone relates to potassium channels. Activation of potassium channels appears to mediate relaxation of cerebral vessels to diverse stimuli including receptor-mediated agonists, intracellular second messengers, and hypoxia. Endothelial- and potassium channel-based mechanisms are related because several endothelium-derived factors produce relaxation by activation of potassium channels. The influence of potassium channels may be altered by disease states including chronic hypertension, subarachnoid hemorrhage, and diabetes. Footnotes Original studies by the authors that are summarized in this review were supported by National Institutes of Health Grants NS-24621, HL-38901, AG-10269, HL-16066, and HL-14355 and American Heart Association Grant-in-Aid 95014510. F. M. Faraci is an Established Investigator of the American Heart Association. Copyright © 1998 the American Physiological Society

Journal

Physiological ReviewsThe American Physiological Society

Published: Jan 1, 1998

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