Journal article
Effect of endogenous vasopressin on blood flow to choroid plexus during hypoxia and intracranial hypertension
American journal of physiology. Heart and circulatory physiology, Vol.266(2), pp.H393-H398
02/01/1994
DOI: 10.1152/ajpheart.1994.266.2.H393
PMID: 8141339
Abstract
Exogenous vasopressin decreases blood flow to the choroid plexus and production of cerebrospinal fluid. Some studies indicate that hypoxia and increases in intracranial pressure (ICP) produce increases in circulating vasopressin. We examined the hypothesis that endogenous release of vasopressin decreases blood flow to the choroid plexus during hypoxia and increased ICP. Blood flow to the choroid plexus was measured in anesthetized rabbits using microspheres. Hypoxia increased cerebral blood flow more than twofold but had little effect on blood flow to the choroid plexus. In contrast, hypoxia produced a marked increase in blood flow to the choroid plexus in the presence of a vasopressin V1-antagonist, [d(CH2)5Tyr(Me)]AVP. During intracranial hypertension, blood flow to the choroid plexus decreased from 409 +/- 42 to 295 +/- 25 ml.min-1 x 100 g-1 (means +/- SE; P < 0.05 vs. control) when ICP was increased from 1 to 40 mmHg. The vasopressin antagonist inhibited the decrease in blood flow to the choroid plexus in response to increased ICP. Thus release of vasopressin during hypoxia and increased ICP have a constrictor effect on blood vessels of the choroid plexus. Plasma levels of vasopressin increased minimally during hypoxia and increased ICP, which suggests that sources of vasopressin other than plasma affect blood vessels of the choroid plexus. We propose that endogenous vasopressin may play a protective role during hypoxia and intracranial hypertension by a negative feedback mechanism to reduce blood flow to the choroid plexus.
Details
- Title: Subtitle
- Effect of endogenous vasopressin on blood flow to choroid plexus during hypoxia and intracranial hypertension
- Creators
- Frank M Faraci - Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242Dale Kinzenbaw - Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242Donald D Heistad - Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.266(2), pp.H393-H398
- DOI
- 10.1152/ajpheart.1994.266.2.H393
- PMID
- 8141339
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Language
- English
- Date published
- 02/01/1994
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040452702771
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