ラット培養血管平滑筋細胞におけるセロトニンの細胞内カルシウム上昇作用機序 Mechanism of serotonin-induced increase in intracellular calcium concentration in rat aortic smooth muscle cells: Effect of Ni^<2+> on extracellular calcium influx

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著者

    • 平藤 雅彦 HIRAFUJI Masahiko
    • 北海道医療大学薬学部薬理学教室 Department of Pharmacology, Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido
    • 根津 顕弘 NEZU Akihiro
    • 北海道医療大学薬学部薬理学教室 Department of Pharmacology, Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido
    • 金井 幸辰 KANAI Yukitatu
    • 北海道医療大学薬学部薬理学教室 Department of Pharmacology, Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido
    • 南 勝 MINAMI Masaru
    • 北海道医療大学薬学部薬理学教室 Department of Pharmacology, Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido

抄録

In cardiovascular system, serotonin (5-hydroxytryptanune; 5-HT) induces very strong vasoconstriction, which is considered to be associated with hypertension or vasospasm. Intracellular calcium ions play a key role as second messenger in the regulation of vasoconstriction. In the present study, we investigated the effect of Ni<SUP>2+</SUP>, a cation chenel inhibitor, on 5-HT-induced increase in intracellular calcium concentration ([Ca<SUP>2+</SUP>]i) using cultured rat aortic smooth muscle cells (VSMCs). VSMCs were obtained by collagenase digestion and seeded on coverglass. Cells were cultured in 95% air and 5% C02 for 8-10 days in Dulbecco's MEM containing 10% fetal calf serum. [Ca<SUP>2+</SUP>]i was measured by a fluorescence spectrophotometer using fura-2. 5-HT (10 μM) caused a biphasic increase in [Ca<SUP>2+</SUP>]i of VSMCs, i.e., transient and tonic increase. Ni<SUP>2+</SUP> (1 mM) significantly inhibited the tonic increase, but had no effect on the transient increase. Ni<SUP>2+</SUP> also suppressed 5-HT-induced increase in IP3 content, suggesting that extracellular calcium influx is involved in the transient increase, in addition to the release from intracellular stores. However, Ni<SUP>2+</SUP> completely inhibited calcium influx through voltagedependent calcium channel induced by high KCl (80 mM). Also, Ni<SUP>2+</SUP> significantly inhibited calcium influx induced by thapsigargin (1 μM). These results suggest that 5-HT induces transient calcium influx through Ni<SUP>2+</SUP> -sensitive calcium channel, which is distinct from voltage-dependent, capacitative or second messengeroperated calcium channels.

収録刊行物

  • 日本薬理学雑誌

    日本薬理学雑誌 106, 202-206, 1995-09-01

    公益社団法人 日本薬理学会

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