Document Detail


Prostacyclin synthesis in relation to sympathoadrenal activation. Effects of beta-blockade.
MedLine Citation:
PMID:  1683609     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Results from several studies suggest that beta-adrenoceptor blockade causes increased biosynthesis of the vasodilator prostanoid prostacyclin in the arterial wall. This effect may contribute to the clinical effects of beta-blockers in hypertension and coronary heart disease. Studies in hypertensive patients and in animals indicate that the arterial pressure reduction after beta-blockade is related to the associated increase of prostacyclin biosynthesis, regarding both magnitude and time of onset of effect. Some observations suggest that the effects of beta-blockers in myocardial ischemia may in part be due to an improvement of coronary blood flow caused by increased prostacyclin biosynthesis.
Authors:
K Pettersson; G Hansson; J A Björkman; B Ablad
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Circulation     Volume:  84     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1991 Dec 
Date Detail:
Created Date:  1992-01-07     Completed Date:  1992-01-07     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  VI38-43     Citation Subset:  AIM; IM    
Affiliation:
Department of Cardiovascular Pharmacology, Astra Hässle AB, Mölndal, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Antagonists / pharmacology*
Animals
Antihypertensive Agents / pharmacology
Epoprostenol / biosynthesis*
Humans
Sympathetic Nervous System / drug effects*,  physiology
Chemical
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Antihypertensive Agents; 35121-78-9/Epoprostenol

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


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