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  • 1
    Electronic Resource
    Electronic Resource
    Analysis of a porcine EP3-receptor: cloning, expression and signal transduction (1998)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 358 (1998), S. 160-167 
    Details
    ISSN: 1432-1912
    Keywords: Key words EP3-receptor ; cAMP ; NFκB ; E-box ; SP1 ; AP2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A cDNA clone, encoding a complete porcine EP3 receptor, was isolated from a porcine heart cDNA library. The deduced amino acid sequence revealed a protein of 387 amino acid residues with an estimated molecular weight of 43 kD and strongest homology to the human EP3-II receptor (84% identity on protein level). Ligand binding studies with transfected COS-7 cells, expressing the porcine receptor, showed displacement of [3H]PGE1 with the EP3-specific agonist M & B 28.767, the EP1/EP3-agonist sulprostone but not with the EP2-specific agonist butaprost. Stimulation of transfected CHO cells with M & B 28.767 resulted in inhibition of forskolin-induced cAMP formation, suggesting coupling to an inhibitory G protein. Agonist-induced translocation of the transcription factor NFκB into the nucleus of transfected CHO cells was demonstrated by Western blot analysis, indicating that these EP3 receptors modulate NFκB-dependent cellular signal transduction. Analysis of the genomic organization identified the major transcription initiation site at about 160 bp upstream of the ATG start codon. The 800-bp 5’ flanking region contains a variety of putative cis-acting regulatory elements, including binding sites for AP2, SP1 and MyoD (E-box). The present data will now allow further studies on EP3 receptor-mediated signal transduction and its regulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005238
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  • 2
    Electronic Resource
    Electronic Resource
    Possible role of prostaglandins in the regulation of coronary blood flow (1981)
    Springer
    Basic research in cardiology 76 (1981), S. 239-249 
    Details
    ISSN: 1435-1803
    Keywords: heart ; myocardial ischemia ; prostacyclin (PGI2) ; thromboxanes ; coronary vessels ; cyclic AMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Prostaglandine können als eine Gruppe chemischer Substanzen angesehen werden, die lokal entstehen und die koronare Perfusion an die Stoffwechselerfordernisse des Herzens anpassen. Vorliegende Arbeit gibt eine Zusammenfassung des heutigen Wissensstandes auf diesem Gebiet unter besonderer Berücksichtigung von Prostacyclin (PGI2). Neben Biosynthese und Metabolismus sowie ihrer Beeinflussung durch Pharmaka werden kardiale und koronare Wirkungen von PGI2 beschrieben und mögliche Wirkungsmechanismen der Substanz unter physiologischen und pathophysiologischen (myokardiale Ischämie) Bedingungen diskutiert. Im Mittelpunkt stehen Wechselwirkungen zwischen PGI2, Adenosin und Katecholaminen und ihre möglichen Konsequenzen für die Regulation des koronaren Tonus. Hierzu wird ein Modell vorgestellt, bei dem die direkt-vasokonstriktorischen und stoffwechselsteigernden Katecholaminwirkungen durch Bildung von PGI2 im Gefäßbereich und Adenosin im Herzmuskelstoffwechsel funktionell antagonisiert werden.
    Notes: Summary Prostaglandins may represent one group of local chemical factors that control coronary perfusion and adapt it to the metabolic demands of the heart. Present study summarizes the current knowledge in this field with particular reference to prostacyclin (PGI2). The major biosynthetic pathways and their modification by drugs are briefly outlined. The sources and fates of cardiac prostaglandins are described and possible mechanisms of action discussed in both physiological and pathophysiological (myocardial ischemia) situations. Attention is focussed on the interplay between catecholamines, adenosine and PGI2. A model is presented, based on the hypothesis that adenosine from myocardial metabolism and PGI2 from vascular sites are acting in concert to antagonize sympathetic metabolic and vasoconstrictory influences and to maintain an adequate blood supply to the heart.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907769
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  • 3
    Electronic Resource
    Electronic Resource
    Inotropic actions of eicosanoids (1992)
    Springer
    Basic research in cardiology 87 (1992), S. 2-11 
    Details
    ISSN: 1435-1803
    Keywords: Prostaglandins ; leukotrienes ; thromboxanes ; myocardialcontraction ; intracellularsignaling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Eicosanoids (prostaglandins, leukotrienes, thromboxane A2 and other metabolites of C-20 polyunsaturated fatty acids) have numerous effects in the cardiovascular system. Direct inotropic actions have been repeatedly described, but appear in only very few cases to be due to direct modification of the inotropic state of the heart. Specific eicosanoid receptors have been identified on the surface of the sarcolemmal membrane. Signal transduction pathways in the cardiac myocyte involve the adenylate cyclase/cAMP system or stimulation of the phospholipase C/IP3 pathway. In general, concentrations of eicosanoids which affect myocardial contractility are higher as the response is less predictable than the effects on platelet function or vessel tone. Therefore, eicosanoid-induced extracardiac effects may be superimposed to more direct changes in the contractile state of the intact heart in vitro or in vivo. In contrast to non-failing hearts, there is a significant improvement of the contractile function in contractile failure (“stunning”, ischemia, congestive heart failure) by vasodilating prostaglandins (e.g., PGI2). The mechanism of this action is still unknown.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00795384
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    Paper (German National Licenses)
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