Effect of ursodeoxycholate on phospholipase C-mediated intracellular signal transduction by ethanol and vasopressin in intact rat hepatocytes.

DOI Web Site 2 Citations
  • AKACHI Kazunori
    First Department of Internal Medicine, Nagoya City University Medical School
  • TSUKADA Katsuhiko
    First Department of Internal Medicine, Nagoya City University Medical School
  • HOSHINO Makoto
    First Department of Internal Medicine, Nagoya City University Medical School
  • NAKAYAMA Yoshihide
    First Department of Internal Medicine, Nagoya City University Medical School
  • HIGASHI Katsuyoshi
    First Department of Internal Medicine, Nagoya City University Medical School
  • NOMURA Tomoyuki
    First Department of Internal Medicine, Nagoya City University Medical School
  • YAMADA Junichi
    First Department of Internal Medicine, Nagoya City University Medical School
  • ISOBE Tomoaki
    First Department of Internal Medicine, Nagoya City University Medical School
  • NAKAO Haruhisa
    First Department of Internal Medicine, Nagoya City University Medical School
  • TAKEUCHI Toshihiko
    First Department of Internal Medicine, Nagoya City University Medical School

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Other Title
  • 肝細胞におけるホスホリパーゼＣ作動性細胞内情報伝達に及ぼすウルソデオキシコール酸の影響　エタノール，ｖａｓｏｐｒｅｓｓｉｎによる検討
  • エタノール,vasopressinによる検討

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Description

The effects of ursodeoxycholate (UDC) and its taurine-conjugated form TUDC on phospholipase C (PLC)-mediated intracellular signal transduction by ethanol (EtOH) and vasopressin were investigated in isolated rat hepatocytes. Vasopressin-induced PLC activation was sustained, but the response to EtOH was transient and a return to the basal value was seen at a 2 min after stimulation. Pretreatment of hepatocytes with UDC or TUDC enhanced EtOH-induced Ca2+ mobilization, but did not affect InsP3 accumulation. In contrast, both Ca2+ mobilization and InsP3 accumulation induced by vasopressin were inhibited by pretreatment with these bile acids. Pretreatment with cholate and taurocholate also inhibited the response to vasopressin. EtOH inhibited the subsequent vasopressininduced Ca2+ mobilization, and combined pretreatment of the cells with a maximum concentration of EtOH (300mM) and UDC/TUDC were additive in inhibiting the response to vasopressin, suggesting that the action sites of UDC is different from those of EtOH in hepatocytes. Thus, these results demonstrated that UDC affects PLC-mediated intracellular signal transduction in hepatocytes.

Journal

  • Kanzo

    Kanzo 35 (2), 146-156, 1994

    The Japan Society of Hepatology

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