Alkalinization-Induced K^+ Current of the Mouse Megakaryocyte

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We have recently found that mouse megakaryocytes responded to extracellular alkalinization to pH>8.0, generating a K<SUP>+</SUP> current under voltage-clamped conditions with the whole cell recording mode of the patch-clamp technique. The purpose of this study was to physiologically and pharmacologically characterize the alkaline-dependent K<SUP>+</SUP> conductance of the megakaryocyte membrane. The alkalinization-induced K<SUP>+</SUP> current (I<SUB>ALK</SUB>) did not seem to be Ca<SUP>2+</SUP>-dependent since I<SUB>ALK</SUB> was allowed to be generated under intracellularly Ca<SUP>2+</SUP>-buffered conditions with 10 mM EGTA, which completely prevented the generation of caffeine-induced Ca<SUP>2+</SUP>-activated currents of mouse megakaryocytes; and no [Ca<SUP>2+</SUP>]<SUB>i</SUB> elevation was evoked by the alkalinization protocol in contrast to a significant increase in [Ca<SUP>2+</SUP>]<SUB>i</SUB> in response to caffeine when [Ca<SUP>2+</SUP>]<SUB>i</SUB> was measured with a fura 2 ratiometry. I<SUB>ALK</SUB> was strongly suppressed with tetraethylammonium (TEA), 4-aminopyridine (4-AP) and streptomycin (SM), but was completely resistant to quinidine (QND). The values of IC<SUB>50</SUB> for the suppression of I<SUB>ALK</SUB> with TEA, 4-AP and SM were 5.6, 0.47 and 1.5 mM, respectively. Voltage-gated K<SUP>+</SUP> currents (I<SUB>K</SUB>) of the same megakaryocyte preparation were weakly suppressed with TEA and 4-AP, while they were significantly suppressed with either SM or QND. These results suggest that mouse megakaryocytes possess K<SUP>+</SUP> conductance that was activated by extracellular alkalinization and that probably differs from conventional K<SUP>+</SUP> conductance in its pharmacological properties.

収録刊行物

  • The Japanese journal of pharmacology

    The Japanese journal of pharmacology 79(3), 343-350, 1999-03-01

    公益社団法人 日本薬理学会

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各種コード

  • NII論文ID(NAID)
    10008682879
  • NII書誌ID(NCID)
    AA00691188
  • 本文言語コード
    ENG
  • 資料種別
    REV
  • ISSN
    00215198
  • NDL 記事登録ID
    4699255
  • NDL 雑誌分類
    ZS51(科学技術--薬学)
  • NDL 請求記号
    Z53-D199
  • データ提供元
    CJP書誌  NDL  J-STAGE 
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