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Research ArticleArticle

Mechanisms of Endothelin-Induced Venoconstriction in Isolated Guinea Pig Mesentery

Ron J. Johnson, Gregory D. Fink and James J. Galligan
Journal of Pharmacology and Experimental Therapeutics May 1999, 289 (2) 762-767;
Ron J. Johnson
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Gregory D. Fink
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James J. Galligan
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Abstract

In the present study, endothelin (ET) agonists and receptor selective antagonists were used to characterize ET receptors mediating constriction in guinea pig mesenteric veins (250–300 μm diameter) in vitro. The contribution of ET-evoked vasodilator release to venous tone was also explored. Computer-assisted video microscopy was used to monitor vein diameter. Endothelin-1 (ET-1), endothelin-3 (ET-3), and sarafotoxin 6c (S6c) produced sustained concentration-dependent contractions with a rank order agonist potency of ET-1 = S6c > ET-3. Indomethacin (1 μM) andNϖ-nitro-l-arginine (100 μM) enhanced ET-1 and S6c responses. The ETA selective antagonists BQ-610 (100 nM) and PD156707 (10 nM) shifted ET-1 concentration-response curves rightward and decreased maximal ET-1 responses, without changing S6c responses. The ETBselective antagonist BQ-788 (100 nM) shifted S6c responses rightward but produced no change in ET-1 responses. Combined application of BQ-788 and BQ-610 or BQ-788 and PD 156707 produced a rightward shift in ET-1 responses that was greater than shifts produced by BQ-610 or PD 156707 alone. In conclusion, smooth muscle in guinea pig mesenteric veins expresses ETA and ETB receptors coupled to contractile mechanisms. Activation of endothelial ETBreceptors results in release of vasodilators, primarily nitric oxide.

Footnotes

  • Send reprint requests to: Ron J Johnson, D.V.M., Department of Pharmacology and Toxicology, B440 Life Sciences Building, Michigan State University, East Lansing, MI 48824. E-mail:johns741{at}pilot.msu.edu

  • ↵1 This work was supported by an All Universities Research Initiation Grant (AURIG) from Michigan State University and National Heart, Lung, and Blood Institute Grant HL 24111

  • Abbreviations:
    BQ-610
    (N,N-hexamethylene)carbamoyl-Leu-d-Trp(CHO)-d-Trp
    BQ-788
    N-cis-2,6-dimethylpiperidinocarbonyl-l-γ-MeLeu-d-Trp (COOCH3)-Nle
    EC50
    half-maximal effective molar concentration
    Emax
    maximum contraction
    ET
    endothelin
    NLA
    Nϖ-nitro-l-arginine
    NO
    nitric oxide
    NOS
    nitric oxide synthase
    PD 156707
    {sodium 2-benzo[1,3]dioxol-5-yl-4-(4-methoxy-phenyl)-4-oxo-3-(3,4,5-trimethoxy-benzyl)-but-2-enoate}
    PGI2
    prostacyclin
    S6c
    sarafotoxin 6c
    VSM
    vascular smooth muscle
    • Received September 11, 1998.
    • Accepted December 28, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 289 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 289, Issue 2
1 May 1999
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Research ArticleArticle

Mechanisms of Endothelin-Induced Venoconstriction in Isolated Guinea Pig Mesentery

Ron J. Johnson, Gregory D. Fink and James J. Galligan
Journal of Pharmacology and Experimental Therapeutics May 1, 1999, 289 (2) 762-767;

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Research ArticleArticle

Mechanisms of Endothelin-Induced Venoconstriction in Isolated Guinea Pig Mesentery

Ron J. Johnson, Gregory D. Fink and James J. Galligan
Journal of Pharmacology and Experimental Therapeutics May 1, 1999, 289 (2) 762-767;
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