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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Further Pharmacological Evidence of Nuclear Factor-κB Pathway Involvement in Bradykinin B1 Receptor-Sensitized Responses in Human Umbilical Vein

Sergio Pablo Sardi, Verónica Rey-Ares, Virginia Andrea Pujol-Lereis, Santiago Alejo Serrano and Rodolfo Pedro Rothlin
Journal of Pharmacology and Experimental Therapeutics June 2002, 301 (3) 975-980; DOI: https://doi.org/10.1124/jpet.301.3.975
Sergio Pablo Sardi
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Verónica Rey-Ares
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Virginia Andrea Pujol-Lereis
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Santiago Alejo Serrano
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Rodolfo Pedro Rothlin
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Abstract

Bradykinin (BK) B1 receptors are thought to exert a pivotal role in maintaining and modulating inflammatory processes. They are not normally present under physiological situations but are induced under physiopathological conditions. In isolated human umbilical vein (HUV), a spontaneous BK B1 receptor up-regulation and sensitization process has been demonstrated. Based on pyrrolidine-dithiocarbamate inhibition, it has been proposed that this phenomenon is dependent on nuclear factor-κB (NF-κB) activation. The aim of this study was to further evaluate the NF-κB pathway involvement on BK B1 receptor sensitization in isolated HUV, using several pharmacological tools. In 5-h incubated rings, either the I-κB kinase inhibitor 3-(4-methylphenylsulfonyl)-2-propenenitrile (Bay 11–7082) or the proteasome activity inhibitor Z-Leu-Leu-Leu-CHO (MG-132) inhibited the development of the BK B1 receptor-sensitized contractile responses. Furthermore, pro-inflammatory cytokine interleukin-6 (IL-6) produced a leftward shift of the concentration-response curve to the BK B1 receptor agonist, whereas anti-inflammatory cytokines interleukin-4 (IL-4) and tumor growth factor-β1 (TGF-β1) produced a rightward shift of the responses to des-Arg9-BK in our preparations. Taken together, these results point to NF-κB as a key intermediary in the activation of the expression of BK B1 receptor-sensitized responses in HUV and support the role of inflammatory mediators in the modulation of this process.

Footnotes

  • ↵1 Current address: Department of Neuroscience, Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston. MA. 02115.

  • ↵2 Current address: Department of Molecular Biology, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077-Goettingen, Germany.

  • This research was supported by grants from the Universidad de Buenos Aires (UBA Grant TM-049) and by the Fundación A. J. Roemmers.

  • Abbreviations:
    BK
    bradykinin
    5-HT
    5-hydroxytryptamine or serotonin
    HUV
    human umbilical vein
    IL
    interleukin
    NF-κB
    nuclear factor-κB
    PDTC
    pyrrolidine-dithiocarbamate
    Bay 11–7082
    3-(4-methylphenylsulfonyl)-2-propenenitrile
    MG-132
    Z-Leu-Leu-Leu-CHO
    TGF-β1
    tumor growth factor-β1
    TNF-α
    tumor necrosis factor-α
    • Received September 17, 2001.
    • Accepted March 4, 2002.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 301 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 301, Issue 3
1 Jun 2002
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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Further Pharmacological Evidence of Nuclear Factor-κB Pathway Involvement in Bradykinin B1 Receptor-Sensitized Responses in Human Umbilical Vein

Sergio Pablo Sardi, Verónica Rey-Ares, Virginia Andrea Pujol-Lereis, Santiago Alejo Serrano and Rodolfo Pedro Rothlin
Journal of Pharmacology and Experimental Therapeutics June 1, 2002, 301 (3) 975-980; DOI: https://doi.org/10.1124/jpet.301.3.975

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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Further Pharmacological Evidence of Nuclear Factor-κB Pathway Involvement in Bradykinin B1 Receptor-Sensitized Responses in Human Umbilical Vein

Sergio Pablo Sardi, Verónica Rey-Ares, Virginia Andrea Pujol-Lereis, Santiago Alejo Serrano and Rodolfo Pedro Rothlin
Journal of Pharmacology and Experimental Therapeutics June 1, 2002, 301 (3) 975-980; DOI: https://doi.org/10.1124/jpet.301.3.975
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