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  • Bovine coronary artery  (2)
  • PGE2  (2)
  • AP2  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Cytotoxic enzyme release and oxygen centered radical formation in human neutrophils are selectively inhibited by E-type prostaglandins but not by PGI2 (1990)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 341 (1990), S. 308-315 
    Details
    ISSN: 1432-1912
    Keywords: Prostacyclins ; PGE1 ; PGE2 ; Superoxide anion generation ; gb-Glucuronidase ; cAMP ; Ca2+ ; Human neutrophils ; Platelet activating factor (PAF) ; FMLP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The action of PGE1, PGE2, PGI2 and iloprost on superoxide anion generation, lysosomal enzyme release, and changes of Ca2+ fluxes in human polymorphonuclear leukocytes (PMN) was studied in vitro. Both PGE-type compounds were equipotent inhibitors of FMLP-and PAF-stimulated superoxide anion generation, β-glucuronidase release (IC50 3–5 μmol/l) and Ca2+ influx while PGI2 and iloprost were ineffective at concentrations up to 10 μmol/l. These inhibitory actions of PGE1 and PGE2 were paralleled by an increase in cAMP level of the PMN while no change occurred with PGI2 and iloprost. None of the prostaglandins affected the initial intracellular Ca2+ liberation after challenge with FMLP or PAF. Preincubation of PMN with PGE1 and PGE2 but not with iloprost resulted in subsequent desensitization against a second administration of these compounds. None of the compounds affected PMN activation produced by arachidonic acid or calcimycin (A 23187). These data demonstrate that PGE-type compounds are effective inhibitors of receptor-mediated (PAF, FMLP) activation of human PMN while prostacyclins are considerably less potent. This suggests that the inhibitory prostaglandin receptor on human PMN belongs to the E-type being functionally different from the inhibitory prostaglandin receptor on human platelets. These results suggest that compounds, such as PGE1 and PGE2 might be superior to prostacyclins to prevent PMN-associated generation of reactive oxygen species and lysosomal enzyme release in situations with endogenous PMN activation, i. e. inflammatory reactions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00180656
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    Paper (German National Licenses)
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  • 2
    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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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    The action of the dihydro derivatives of prostacyclin —(6R)-PGI1 and (6S)-PGI1 on the heart and the coronary vasculature (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 306 (1979), S. 213-217 
    Details
    ISSN: 1432-1912
    Keywords: Dihydro-PGI2 ; Prostacyclin (PGI2) ; Bovine coronary artery ; Guinea pig heart ; Myocardial mechanics ; Coronary vascular tone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The action of the dihydro prostacyclins, (6R)-PGI1 and (6S)-PGI1, was studied on the isolated guinea pig heart and bovine coronary artery strips. PGE2 and PGI2 were used as standards. In the isolated guinea pig heart (6S)-PGI1 decreased the coronary perfusion pressure (CPP), myocardial force of contraction (MFC) and oxygen consumption (QO2). (6R)-PGI1 did not produce a significant change in these parameters. The ED50 (50% of maximum coronary dilation) was approximately 20 times higher for (6S)-PGI1 than for PGI2 or PGE2. Treatment of the hearts with reserpine + tyramine abolished the (6S)-PGI1-induced decrease in MFC but not the decrease in the CPP. The same pattern of responses was seen with PGE2. Bovine coronary artery strips were contracted by both (6S)-PGI1 and (6R)-PGI1, the ED50 (50% of maximum increase in tension) being 5 and 10 times higher than that for PGE2. The (6S)-PGI1-induced contraction was preceeded by a small relaxation, which, however, was much less than that seen after PGI2. It is concluded that the hydration of the 5,6 double bound in the PGI2-like activity and generates PGE-like activity. The same biological activity of both dihydro prostacyclins in the isolated coronary artery strip but not in the intact coronary vascular bed leads to suggest that the sites of action in these systems are different.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00507106
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Different sensitivities of prostaglandin-cyclooxygenases in blood platelets and coronary arteries against non-steroidal antiinflammatory drugs (1980)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 313 (1980), S. 69-75 
    Details
    ISSN: 1432-1912
    Keywords: Thromboxane A2 (TXA2) ; Prostacyclin (PGI2) ; Human platelets ; Bovine coronary artery ; Non-steroidal antiinflammatory drugs ; Prostaglandin-cyclooxygenase ; Bioassay ; RCS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The action of the non-steroidal antiinflammatory drugs indomethacin, tiaprofenic acid, diclofenac and meclofenamate on vascular and plateletcyclooxygenases was studied by measuring the arachidonic acid-induced thromboxane A2 (TXA2)-formation of washed human platelets and prostacyclin (PGI2)-formation of bovine coronary artery rings. TXA2 was bioassayed as RCS on rabbit aorta strips, PGI2 in terms of its antiaggregatory activity on ADP-induced aggregation of human platelet-rich plasma. All of the substances studied produced concentration-dependent inhibition of PGI2- and RCS-release. The IC50 [μM] in inhibition of RCS-formation was 0.019 for indomethacin, 0.070 for tiaprofenic acid but 44.9 for meclofenamate and 63.2 for diclofenac. The IC50 [μM] in inhibition of PGI2-release was 0.42 for diclofenac, 0.63 for indomethacin and 0.99 for tiaprofenic acid. The data suggest (1) high sensitivity of human platelet-cyclooxygenase against indomethacin and tiaprofenic acid, (2) different sequence of the substances studied in inhibiting arachidonic acid-induced TXA2- and PGI2-formation. The possible therapeutic value of selective inhibition of platelets and vascular cyclooxygenases in discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00505806
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Increased prostacyclin release from perfused hearts of acutely diabetic rats (1980)
    Springer
    Diabetologia 18 (1980), S. 391-394 
    Details
    ISSN: 1432-0428
    Keywords: Prostaglandins ; prostacyclin ; PGE2 ; perfused rat heart ; prostaglandin endoperoxides ; coronary flow ; platelet aggregation ; streptozotocin diabetes ; bioassay
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The release of prostacyclin and PGE2 from the isolated perfused hearts of acutely diabetic (streptozotocin 100 mg/kg) rats was studied and compared with hearts from control animals. Prostacyclin and PGE2 were measured by a differential bioassay technique. No basal release of either prostaglandin was detected. However, after addition of arachidonic acid, a dose dependent release of prostacyclin and PGE2 was noted. Prostacyclin was identified as the major prostaglandin. Release of prostacyclin and PGE2 from acutely diabetic rat hearts was increased 2–3 times compared to control hearts. No release of prostaglandin endoperoxides was observed in either group of hearts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00276820
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    Paper (German National Licenses)
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