Document Detail


Role of cardiac output in ethanol-evoked attenuation of centrally mediated hypotension in conscious rats.
MedLine Citation:
PMID:  9260994     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Our previous studies have shown that ethanol selectively counteracts centrally mediated hypotensive responses. This study investigated the role of cardiac output and peripheral resistance in the antagonistic interaction between ethanol and antihypertensive drugs. Changes in blood pressure, heart rate, cardiac index, stroke volume, and peripheral resistance elicited by clonidine and subsequent ethanol or saline administration were evaluated in conscious rats. The aortic barodenervated rat was employed because it exhibits greater hypotensive responses to clonidine compared with the intact rat. Aortic barodenervation elicited acute rises in blood pressure, heart rate, and peripheral resistance, whereas cardiac index and stroke volume were not altered. The blood pressure of conscious aortic barodenervated rats returned to sham-operated levels by 48 hours due to concomitant reductions in cardiac index and stroke volume; the peripheral resistance, however, remained significantly elevated. Clonidine (30 microg/kg, I.V.) elicited greater decreases in blood pressure in aortic barodenervated compared with sham-operated rats. The hypotension was caused by decreases in cardiac index and stroke volume because peripheral resistance did not change. Ethanol (1 g/kg, I.V.) counteracted the hypotensive effect of clonidine and raised blood pressure to levels higher than preclonidine values. Significant (P<.05) increases in cardiac index and stroke volume and decreases in peripheral resistance accompanied the pressor effect of ethanol. Additional control groups were included in the study to determine the selectivity of the interaction. A dose of hydralazine (0.5 mg/kg, I.V.) was used that produced similar hypotension to that evoked by clonidine in aortic barodenervated rats. Hydralazine-evoked hypotension was similar in denervated and control rats and resulted from significant reductions in peripheral resistance. Reflex increases in heart rate and stroke volume and hence cardiac output were observed. Ethanol given after hydralazine produced a short-lived pressor effect (<5 minutes versus 40 minutes in the case of clonidine) and counteracted the sympathetically mediated increases in cardiac output, stroke volume, and heart rate. These findings support our hypothesis that ethanol selectively counteracts hypotensive responses of central origin by reversing the reduction in cardiac output elicited by clonidine.
Authors:
M M El-Mas; A A Abdel-Rahman
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Hypertension     Volume:  30     ISSN:  0194-911X     ISO Abbreviation:  Hypertension     Publication Date:  1997 Aug 
Date Detail:
Created Date:  1997-09-11     Completed Date:  1997-09-11     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  288-94     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antihypertensive Agents / pharmacology
Brain / physiology*
Cardiac Output / physiology*
Clonidine / pharmacology
Ethanol / pharmacology*
Hemodynamics / drug effects
Hydralazine / pharmacology
Hypotension / physiopathology*
Male
Rats
Rats, Sprague-Dawley
Grant Support
ID/Acronym/Agency:
AA07839/AA/NIAAA NIH HHS
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 4205-90-7/Clonidine; 64-17-5/Ethanol; 86-54-4/Hydralazine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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