Journal article
Regulation of Cerebral Blood Vessels by Humoral and Endothelium-Dependent Mechanisms Update on Humoral Regulation of Vascular Tone
Hypertension (Dallas, Tex. 1979), Vol.17(6, Part 2), pp.917-922
06/1991
DOI: 10.1161/01.HYP.17.6.917
PMID: 2045173
Abstract
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. (Hypertension 1991;17:917-922)
Details
- Title: Subtitle
- Regulation of Cerebral Blood Vessels by Humoral and Endothelium-Dependent Mechanisms Update on Humoral Regulation of Vascular Tone
- Creators
- Frank Faraci - Departments of Internal Medicine and Pharmacology, Cardiovascular Center, and Veterans Administration Medical Center, University of Iowa College of Medicine, Iowa City, Iowa. Original studies were supported by grants HL-38901, HL-16066, NS-24621, HL-14388, and HL-14230 from the National Institutes of Health; by a Medical Investigatorship and research funds from the Veterans Administration; and by grant IA-90-G-5 from the Iowa Affiliate of the American Heart Association. F.M.F. is an Established Investigator of the American Heart AssociationDonald Heistad
- Resource Type
- Journal article
- Publication Details
- Hypertension (Dallas, Tex. 1979), Vol.17(6, Part 2), pp.917-922
- Publisher
- American Heart Association, Inc
- DOI
- 10.1161/01.HYP.17.6.917
- PMID
- 2045173
- ISSN
- 0194-911X
- eISSN
- 1524-4563
- Language
- English
- Date published
- 06/1991
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040361502771
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