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Inhibitory effects of a selective endothelin-A receptor antagonist YM598 on endothelin-1-induced potentiation of nociception in formalin-induced and prostate cancer-induced pain models in mice.

Inhibitory effects of a selective endothelin-A receptor antagonist YM598 on endothelin-1-induced potentiation of nociception in formalin-induced and prostate cancer-induced pain models in mice. Research Abstract Details 

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  • Inhibitory effects of a selective endothelin-A receptor antagonist YM598 on endothelin-1-induced potentiation of nociception in formalin-induced and prostate cancer-induced pain models in mice. Abstract Text:

    hironori yuyamaHironori Yuyama,akiko koakutsuAkiko Koakutsu,noriko fujiyasuNoriko Fujiyasu,akira fujimoriAkira Fujimori,shuichi satoShuichi Sato,kumiko shibasakiKumiko Shibasaki,shohei tanakaShohei Tanaka,katsumi sudohKatsumi Sudoh,masao sasamataMasao Sasamata,keiji miyataKeiji Miyata,

    In some diseases in which endothelin-1 (ET-1) production increases (e.g. prostate cancer), ET-1 is considered to be involved in the generation of pain. In the present study, we investigated the effects of a selective endothelin-A receptor antagonist, YM598, on the nociception potentiated by ET-1 in formalin-induced and cancer inoculation-induced pain models in mice. The formalin-induced pain model was prepared by intraplantar injection of 0.7% formalin into the hind paws of ICR mice, and the cancer pain model was prepared by inoculation of the human prostate cancer cell line PPC-1 into the hind paws of severe combined immunodeficiency mice. Formalin caused a biphasic pain response and paw edema in the mouse hind paw. ET-1 (10 pmol/paw) potentiated these responses, and single oral administration of YM598 (0.3-3 mg/kg) significantly inhibited this ET-1-induced potentiation of nociception and paw edema. ET-1 (10 pmol/paw) also potentiated the pain response in prostate cancer-inoculated mice. Both YM598 and atrasentan (0.3-3 mg/kg) significantly inhibited the ET-1-induced potentiation of nociception. These results suggest that selective endothelin-A receptor antagonists relieve pain in patients with various diseases in which ET-1 production increases (e.g. prostate cancer).

    Inhibitory effects of a selective endothelin-A receptor antagonist YM598 on endothelin-1-induced potentiation of nociception in formalin-induced and prostate cancer-induced pain models in mice. Publishing Authors By Initials

    h yuyamaH Yuyama,a koakutsuA Koakutsu,n fujiyasuN Fujiyasu,a fujimoriA Fujimori,s satoS Sato,k shibasakiK Shibasaki,s tanakaS Tanaka,k sudohK Sudoh,m sasamataM Sasamata,k miyataK Miyata,

    For similar abstracts research abstracts see: abstracts research

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    Inhibitory effects of a selective endothelin-A receptor antagonist YM598 on endothelin-1-induced potentiation of nociception in formalin-induced and prostate cancer-induced pain models in mice. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Journal of cardiovascular pharmacology

    VOLUME: 44 Suppl 1

    Page Numbers: S479-82

    Journal Abbreviation: J. Cardiovasc. Pharmacol.

    ISSN: 1533-4023

    DAY: 19

    MONTH: Nov

    YEAR: 2004

    Inhibitory effects of a selective endothelin-A receptor antagonist YM598 on endothelin-1-induced potentiation of nociception in formalin-induced and prostate cancer-induced pain models in mice. Information

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    LANGUAGE: eng

    NlmUniqueID: 7902492

    Inhibitory effects of a selective endothelin-A receptor antagonist YM598 on endothelin-1-induced potentiation of nociception in formalin-induced and prostate cancer-induced pain models in mice. Keywords Mesh Terms:

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    Grant and Affiliation Information for Inhibitory effects of a selective endothelin-A receptor antagonist YM598 on endothelin-1-induced potentiation of nociception in formalin-induced and prostate cancer-induced pain models in mice.

    AFFILIATION: Pharmacology Laboratories, Institute for Drug Discovery Research, Yamanouchi Pharmaceutical Co., Ltd, Tsukuba-shi, Ibaraki, Japan. yuyama@yamanouchi.co.jp

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: J Cardiovasc Pharmacol

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