Document Detail

Cardiac and renal prostaglandin I2. Biosynthesis and biological effects in isolated perfused rabbit tissues.
MedLine Citation:
PMID:  346605     Owner:  NLM     Status:  MEDLINE    
Both the isolated perfused rabbit heart and kidney are capable of synthesizing prostaglandin (PG) I(2). The evidence that supports this finding includes: (a) radiochemical identification of the stable end-product of PGI(2), 6-keto-PGF(1alpha), in the venous effluent after arachidonic acid administration; (b) biological identification of the labile product in the venous effluents which causes relaxation of the bovine coronary artery assay tissue and inhibition of platelet aggregation; and (c) confirmation that arachidonic acid and its endoperoxide PGH(2), but not dihomo-gamma-linolenic acid and its endoperoxide PGH(1), serve as the precursor for the coronary vasodilator and the inhibitor of platelet aggregation. The rabbit heart and kidney are both capable of converting exogenous arachidonate into PGI(2) but the normal perfused rabbit kidney apparently primarily converts endogenous arachidonate (e.g., generated by stimulation with bradykinin, angiotensin, ATP, or ischemia) into PGE(2); while the heart converts endogenous arachidonate primarily into PGI(2). Indomethacin inhibition of the cyclo-oxygenase unmasks the continuous basal synthesis of PGI(2) by the heart, and of PGE(2) by the kidney. Cardiac PGI(2) administration causes a sharp transient reduction in coronary perfusion pressure, whereas the intracardiac injection of the PGH(2) causes an increase in coronary resistance without apparent cardiac conversion to PGI(2). The perfused heart rapidly degrades most of the exogenous endoperoxide probably into PGE(2), while exogenous PGI(2) traverses the heart without being metabolized. The coronary vasoconstriction produced by PGH(2) in the normal perfused rabbit heart suggests that the endoperoxide did not reach the PGI(2) synthetase, whereas the more lipid soluble precursor arachidonic acid (exogenous or endogenous) penetrated to the cyclooxygenase, which apparently is tightly coupled to the PGI(2) synthetase.
P Needleman; S D Bronson; A Wyche; M Sivakoff; K C Nicolaou
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  61     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1978 Mar 
Date Detail:
Created Date:  1978-06-12     Completed Date:  1978-06-12     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  839-49     Citation Subset:  AIM; IM    
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MeSH Terms
Biological Assay
Carbon Radioisotopes / diagnostic use
Epoprostenol / biosynthesis*,  pharmacology
Isotope Labeling
Kidney / metabolism*
Muscle Contraction / drug effects
Muscle, Smooth / drug effects
Myocardium / metabolism*
Platelet Aggregation / drug effects
Prostaglandins / biosynthesis*
Prostaglandins H / pharmacology
Reg. No./Substance:
0/Carbon Radioisotopes; 0/Prostaglandins; 0/Prostaglandins H; 35121-78-9/Epoprostenol

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

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