| Central nervous system mediates an antihypertensive property in glucocorticoid hypertension in dogs. | |
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MedLine Citation:
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PMID: 8586809 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: To determine whether the central nervous system has a pressor or a depressor role in glucocorticoid-induced hypertension. METHODS: Intracerebroventricular dexamethasone or its receptor antagonist, RU 38486, was administered in 20 trained conscious dogs. In addition, intracerebroventricular RU 38486 was administered in dogs treated with oral dexamethasone. RESULTS: Intracerebroventricular dexamethasone induced a dose-related reduction in blood pressure accompanied by decreased heart rate and cardiac output. In contrast, intracerebroventricular RU 38486 caused a slight but not significant elevation in blood pressure. Total peripheral resistance showed no significant change throughout the treatment with dexamethasone or RU 38486. In contrast, oral dexamethasone caused significant elevation of blood pressure associated with increased total peripheral resistance and reduced heart rate. In hypertensive dogs treated with oral dexamethasone, intracerebroventricular RU 38486 elicited a more severe form of hypertension accompanied by an attenuation of the heart rate and a reduction in cardiac output. Intracerebroventricular dexamethasone induced a significant reduction in plasma levels of adrenocorticotrophic hormone, cortisol, arginine vasopressin and noradrenaline. In addition, simultaneous central administration of RU 38486 with intracerebroventricular dexamethasone blocked the reduction in blood pressure and heart rate completely. CONCLUSION: The present data strongly suggest that endogenous glucocorticoid in the central nervous system may not have a role in the regulation of systemic haemodynamics and hormones under resting conditions, but does play an important part during the glucocorticoid excess state, for example glucocorticoid hypertension caused by oral treatment with dexamethasone. The glucocorticoid in the central nervous system opposed the elevation of blood pressure in glucocorticoid-induced hypertension by attenuating the reduction in heart rate and cardiac output via direct stimulation of glucocorticoid receptors in the brain. |
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Authors:
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H Nakamoto; H Suzuki; Y Kageyama; M Murakami; M Naitoh; T Saruta |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Journal of hypertension Volume: 13 ISSN: 0263-6352 ISO Abbreviation: J. Hypertens. Publication Date: 1995 Oct |
Date Detail:
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Created Date: 1996-03-27 Completed Date: 1996-03-27 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8306882 Medline TA: J Hypertens Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 1169-79 Citation Subset: IM |
Affiliation:
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Kidney Disease and Dialysis Center, Saitama Medical School, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Central Nervous System / drug effects*, physiopathology Dexamethasone / pharmacology* Dogs Glucocorticoids / pharmacology* Hemodynamics Hormone Antagonists / pharmacology Hypertension / chemically induced*, metabolism, physiopathology Male Mifepristone / pharmacology Receptors, Glucocorticoid / drug effects, physiology |
| Chemical | |
Reg. No./Substance:
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0/Glucocorticoids; 0/Hormone Antagonists; 0/Receptors, Glucocorticoid; 50-02-2/Dexamethasone; 84371-65-3/Mifepristone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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