Hypertension, Vol 17, 917-922, Copyright © 1991 by American Heart Association
FM Faraci and DD Heistad
Recent studies suggest that humoral and endothelium-dependent mechanisms
may play an important role in the cerebral circulation. Angiotensin may
acutely and chronically increase resistance of large cerebral arteries and
reduce cerebral microvascular pressure without changing cerebral blood
flow. We hypothesize that the brain may sense reductions in microvascular
pressure and initiate compensatory neurohumoral responses to raise arterial
pressure. Vasopressin appears to play an important role in regulation of
production of cerebrospinal fluid and brain fluid volume. Vasopressin also
may be protective when intracranial pressure is elevated.
Endothelium-dependent mechanisms also may have important influences on tone
of cerebral vessels. Synthesis of the endothelium-derived relaxing factor
nitric oxide, or a nitric oxide-containing compound, appears to influence
both basal tone and responses of large cerebral arteries to acetylcholine
in vivo. Large cerebral arteries dilate in response to increased blood flow
in vivo, and this response may be mediated in part by release of a humoral
factor by endothelium. Endothelium-dependent responses of cerebral
arterioles to receptor- and nonreceptor-mediated agonists are impaired
during chronic hypertension. The mechanism of impairment of endothelium-
dependent responses of cerebral arterioles appears to involve production of
an endothelium-derived contracting factor.
ARTICLES
Regulation of cerebral blood vessels by humoral and endothelium- dependent mechanisms. Update on humoral regulation of vascular tone
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
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