Document Detail


The alpha2 -adrenergic receptors in hypertension and heart failure: experimental and clinical studies.
MedLine Citation:
PMID:  11725152     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This is a brief overview of experimental and clinical studies exploring the hemodynamic functions of the alpha2A and alpha2B adrenergic receptor (AR) subtypes in animals submitted to genetic manipulations or gene treatment, as well as the clinical effects of central sympathetic suppression with the alpha2-AR agonist clonidine in patients with ischemic heart disease and/or heart failure. The animal experiments have led us to conclude that the sympathetic outflow is regulated by activation of the presynaptic alpha2A-AR subtype, which is the predominant alpha2-AR subtype in the central nervous system and exerts a sympathoinhibitory (hypotensive) action; on the contrary, activation of the central alpha2B-AR elicits a sympathoexcitatory response (such as seen in salt-induced hypertension, which requires functionally intact alpha2B-AR). Since there are no selective pharmacologic agents yet capable of discriminating among alpha2-AR subtypes, clinical studies utilize clonidine, the central sympathetic suppressant effect of which has been used for 35 years to treat hypertension. In small clinical trials, clonidine was used successfully for treatment of acute or chronic heart failure, acute myocardial infarct or hypertensive cardiomyopathy with subclinical diastolic dysfunction. We speculate that future development of agents capable of selectively activating the alpha2A-AR or blocking the alpha2B-AR may further improve our capability to treat hypertension, ischemic heart disease and heart failure.
Authors:
I Gavras; A J Manolis; H Gavras
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Journal of hypertension     Volume:  19     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  2001 Dec 
Date Detail:
Created Date:  2001-11-28     Completed Date:  2002-02-07     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  2115-24     Citation Subset:  IM    
Affiliation:
Hypertension and Atherosclerosis Section of the Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Agonists / therapeutic use
Animals
Arteries / physiopathology
Blood Pressure / physiology
Brain / physiopathology
Cardiac Output, Low / physiopathology*
Gene Deletion
Gene Expression
Gene Therapy
Humans
Hypertension / physiopathology*,  therapy
Receptors, Adrenergic, alpha / genetics,  physiology*
Grant Support
ID/Acronym/Agency:
P50 HL55001/HL/NHLBI NIH HHS; R01 HL46693/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic alpha-Agonists; 0/Receptors, Adrenergic, alpha

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


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