Document Detail

Adenosine receptor-mediated alterations in prostacyclin production and cardiac function in the isolated rabbit heart.
MedLine Citation:
PMID:  1578377     Owner:  NLM     Status:  MEDLINE    
The subtype of adenosine receptor linked to cardiac prostacyclin (PGI2) synthesis, measured as immunoreactive 6-keto-PGF1 alpha, was investigated in the rabbit heart perfused with Krebs' buffer at 20 ml/min. Adenosine (6.4-50 nmol) decreased 6-keto-PGF1 alpha synthesis, coronary perfusion pressure (PP) and myocardial contractility (dp/dt max), whereas higher doses (200 nmol) increased 6-keto-PGF1 alpha output and decreased PP, heart rate (HR) and dp/dt max. Injections (3.2-50 nmol) or infusion (0.6 microM) of A1 receptor agonist 1-deaza,2-chloro,N6 cyclopentyladenosine increased 6-keto-PGF1 alpha production and decreased HR and PP without affecting dp/dt max. 1-Deaza,2-chloro,N6 cyclopentyladenosine 100 to 200 nmol produced similar effects as lower doses except that it decreased transiently PP and reduced dp/dt max. 1,3-Dipropyl,8-cyclopentylxanthine (0.06 microM) prevented the effects of 1-deaza,2-chloro,N6 cyclopentyladenosine (50 mumol) and adenosine (10 microM) to increase 6-keto-PGF1 alpha output and decrease HR and minimized the decrease in dp/dt max. A2 receptor agonist 2-[p-(2-carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamido-ade nos ine (1.6-12.5 nmol) or 0.6 microM decreased 6-keto-PGF1 alpha output, PP and dp/dt max without changes in HR. 3,7-Dimethyl-1-propargylxanthine prevented 2-[p-(2-carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamido adenosine-induced decrease in 6-keto-PGF1 alpha output, PP and dp/dt max; HR was not altered by this agent. These data suggest that stimulation of A2 receptors reduce cardiac PGI2 synthesis and PP, but activation of A1 adenosine receptors increased PGI2 synthesis, produced vasoconstriction and decreased HR.(ABSTRACT TRUNCATED AT 250 WORDS)
C Cano; K U Malik
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of pharmacology and experimental therapeutics     Volume:  261     ISSN:  0022-3565     ISO Abbreviation:  J. Pharmacol. Exp. Ther.     Publication Date:  1992 May 
Date Detail:
Created Date:  1992-06-05     Completed Date:  1992-06-05     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0376362     Medline TA:  J Pharmacol Exp Ther     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  660-8     Citation Subset:  IM    
Department of Pharmacology, School of Medicine, University of Tennessee, Memphis.
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MeSH Terms
6-Ketoprostaglandin F1 alpha / metabolism
Adenosine / analogs & derivatives*,  pharmacology*
Antihypertensive Agents / pharmacology
Dose-Response Relationship, Drug
Epoprostenol / biosynthesis*
Heart / drug effects*
Heart Rate / drug effects
Myocardial Contraction / drug effects
Myocardium / metabolism*
Phenethylamines / pharmacology*
Receptors, Purinergic / drug effects*
Theobromine / analogs & derivatives,  pharmacology
Grant Support
19134//PHS HHS
Reg. No./Substance:
0/Antihypertensive Agents; 0/Phenethylamines; 0/Receptors, Purinergic; 113646-62-1/1-deaza-2-chloro-N(6)-cyclopentyladenosine; 120225-54-9/CGS 21680; 14114-46-6/3,7-dimethyl-1-propargylxanthine; 35121-78-9/Epoprostenol; 58-61-7/Adenosine; 58962-34-8/6-Ketoprostaglandin F1 alpha; 83-67-0/Theobromine

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

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