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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 306 (1979), S. 101-103 
    ISSN: 1432-1912
    Keywords: Prostacyclin (PGI2) ; Cyclic AMP ; Adenosine ; Noradrenaline ; Coronary arteries
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of prostacyclin (PGI2) on vascular tension and cAMP content were measured in isolated bovine coronary artery strips. 3 nM PGI2 did not alter the tension but diminished the cAMP content by 56% of the control level (P〈0.005). 30 and 300 nM PGI2 diminished the tension and further reduced the cAMP content, which amounted to only 5% of the control at 300 nM PGI2. These results are in contrast to the increase in cAMP level by PGI2 in blood platelets and might indicate a different mechanism of action of PGI2 in platelets and vascular tissue.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 357 (1997), S. 10-16 
    ISSN: 1432-1912
    Keywords: Key words Thromboxane A2 receptor ; Cloning ; Expression ; Radioligand binding ; Cyclic AMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study describes the molecular cloning and functional characterization of the bovine thromboxane A2 (TP) receptor. Two partial nucleotide sequences coding for the bovine TP receptor were isolated from a bovine genomic and a bovine heart cDNA library. The deduced amino acid sequence suggests a heptahelical protein of 343 amino acids. The receptor protein is homologous with that of human placenta and endothelium at 84.0% and 81.4%, respectively. COS-7 cells were transfected with the bovine TP receptor cDNA, and binding affinities were assessed by radioligand binding studies. Specific displacement of [3H]SQ 29548 was demonstrated in COS-7 cell membranes with the unlabeled TP receptor antagonist SQ 29548 (K d = 12.6 ± 1.1 nM) and the TP receptor agonist U46619 (K d = 192.1 ± 58.9 nM), but not with other prostaglandins (PGD2, PGE1, PGF2α), or the PGI2 mimetic cicaprost. Agonist-induced stimulation of adenylyl cyclase in transfected COS-7 cells indicates a linkage to the cAMP signal transduction pathway via coupling to a stimulatory G-protein. Since bovine cells, e.g. vascular smooth muscle cells, are an established model to study the role of eicosanoids in cell signaling, this report on the molecular structure of the bovine TP receptor will allow further studies on receptor regulation.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 76 (1981), S. 239-249 
    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
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  • 4
    ISSN: 1435-1803
    Keywords: prostacyclin ; thromboxane ; platelets ; coronary vessels ; arachidonic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A new experimentalin-vitro model is described, which was used for studying prostacyclin (PGI2)-thromboxane A2 (TXA2)-interactions. Langendorff hearts of guinea pigs are perfused at constant volume with Krebs-Henseleit buffer and washed human platelets (4x108/min). PGI2 and TXA2 release are measured by bioassay. The cardiac and coronary function and the myocardial oxygen consumption are continuously monitored. The platelet count in the cardiac effluent can be measured and the cAMP content has been estimated. This model might be a useful tool for studying the roles of PGI2 and TXA2 in platelet activation and coronary perfusion in terms of endogenously synthesized substances.
    Type of Medium: Electronic Resource
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