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OtherCARDIOVASCULAR PHARMACOLOGY

Characterization of Endothelium-Dependent Relaxation Independent of NO and Prostaglandins in Guinea Pig Coronary Artery

Akihiro Yamanaka, Tomohisa Ishikawa and Katsutoshi Goto
Journal of Pharmacology and Experimental Therapeutics May 1998, 285 (2) 480-489;
Akihiro Yamanaka
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Tomohisa Ishikawa
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Katsutoshi Goto
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Abstract

In the presence of Nω-nitro-l-arginine and indomethacin, acetylcholine (ACh) induced endothelium-dependent relaxation in guinea pig coronary artery preconstricted with 9,11-dideoxy-9α,11α-epoxymethano prostaglandin F2α. Dexamethasone and arachidonyltrifluoromethyl ketone, inhibitors of phospholipase A2, and 17-octadecynoic acid, an inhibitor of cytochrome P450 epoxygenase, had no effect on the response to ACh. Although proadifen, which is used widely as an inhibitor of cytochrome P450-dependent enzymes, suppressed the ACh-induced relaxation, the drug also inhibited the relaxation induced by cromakalim, a K+channel opener. In isolated smooth muscle cells of guinea pig coronary artery, proadifen, but not 17-octadecynoic acid, almost abolished delayed rectifier K+ current. Epoxyeicosatrienoic acids failed to relax the artery. Apamin and iberiotoxin, inhibitors of small- and large-conductance Ca++-activated K+channels, respectively, did not affect the relaxation induced by ACh. A combination of charybdotoxin plus apamin, but not iberiotoxin plus apamin, abolished the response. However, the combination of charybdotoxin plus apamin had no effect on ACh-induced increase in intracellular free Ca++ concentration in endothelial cells. These results suggest that epoxyeicosatrienoic acids do not contribute to Nω-nitro-l-arginine/indomethacin-resistant relaxation induced by ACh in the guinea pig coronary artery. The present study also proposes that K+ channels on vascular smooth muscle cells, which both charybdotoxin and apamin must affect for inhibition to occur, are the target for endothelium-derived hyperpolarizing factor.

Footnotes

  • Send reprint requests to: Katsutoshi Goto, Ph.D., Department of Pharmacology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba, Ibaraki 305–8575, Japan.

  • ↵1 This study was supported by a grant-in-aid for scientific research from the Ministry of Education, Science and Culture of Japan, and Uehara Memorial Foundation.

  • Abbreviations:
    l-NNA
    Nω-nitro-l-arginine
    ACh
    acetylcholine
    NO
    nitric oxide
    ChTX
    charybdotoxin
    IbTX
    iberiotoxin
    4-AP
    4-aminopyridine
    17-ODYA
    17-octadecynoic acid
    TEA
    tetraethylammonium chloride
    EDHF
    endothelium-derived hyperpolarizing factor
    PLA2
    phospholipase A2
    EET
    epoxyeicosatrienoic acid
    U-46619
    9,11-dideoxy-9α,11α-epoxymethano-prostaglandin F2α
    AACOCF3
    arachidonyltrifluoromethyl ketone
    BKca
    large-conductance Ca++-activated K+ channel
    SKca
    small-conductance Ca++-activated K+ channel
    KATP
    ATP-sensitive K+ channel
    Kdr
    delayed rectifier K+ channel
    IKca
    intermediate-conductance Ca++-activated K+channel
    EGTA
    ethyleneglycol-bis(β-aminoethyl ether)-N,N,N′,N′-tetraacetic acid
    HEPES
    N-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid
    • Received September 29, 1997.
    • Accepted January 9, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 285, Issue 2
1 May 1998
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OtherCARDIOVASCULAR PHARMACOLOGY

Characterization of Endothelium-Dependent Relaxation Independent of NO and Prostaglandins in Guinea Pig Coronary Artery

Akihiro Yamanaka, Tomohisa Ishikawa and Katsutoshi Goto
Journal of Pharmacology and Experimental Therapeutics May 1, 1998, 285 (2) 480-489;

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OtherCARDIOVASCULAR PHARMACOLOGY

Characterization of Endothelium-Dependent Relaxation Independent of NO and Prostaglandins in Guinea Pig Coronary Artery

Akihiro Yamanaka, Tomohisa Ishikawa and Katsutoshi Goto
Journal of Pharmacology and Experimental Therapeutics May 1, 1998, 285 (2) 480-489;
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