Ca2+‐dependent aggregation of rabbit platelets induced by maitotoxin, a potent marine toxin, isolated from a dinoflagellate

Akiko Watanabe, Yukisato Ishida, Hiromi Honda, Masaki Kobayashi, Yasushi Ohizumi

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19 Citations (Scopus)


Administration of maitotoxin (MTX), a dinoflagellate toxin, caused aggregation of rabbit washed platelets. The cytosolic Ca2+ concentration ([Ca2+]i), measured by fura‐2 fluorescence technique, was also increased by the presence of MTX. Rates of aggregation response and [Ca2+]i‐increase were dependent on tested concentrations (3–100 ng ml−1) of the toxin. The MTX‐induced platelet aggregation and [Ca2+]i‐increase were totally abolished in a Ca2+‐free solution. The successive administration of Ca2+ in the presence of MTX elicited the aggregation and increase in [Ca2+]i. Ba2+ was capable of substituting for Ca2+ in the MTX‐induced platelet aggregation. In the presence of external Ca2+, transition metals, Co2+, Cd2+ and Ni2+, inhibited the aggregation response to MTX. Organic calcium antagonists (verapamil and nifedipine) as well as a cyclo‐oxygenase‐inhibitor (aspirin) did not apparently inhibit the aggregation response to MTX, except for a high concentration (10−5 m) of verapamil, while procaine (10 mm) reduced the rate of platelet aggregation. MTX also elicited a release of ATP from platelets, which was abolished in the absence of external Ca2+. In contrast, thrombin 0.5 unit ml−1 could elicit platelet shape change, [Ca2+]i‐increase and ATP‐release in the absence of external Ca2+. These results suggest that the MTX‐induced platelet activation is caused by an enhanced Ca2+‐influx presumably through voltage‐independent Ca2+ channels on the plasma membrane. 1993 British Pharmacological Society

Original languageEnglish
Pages (from-to)29-36
Number of pages8
JournalBritish Journal of Pharmacology
Issue number1
Publication statusPublished - 1993 May
Externally publishedYes


  • Maitotoxin
  • aggregation
  • cytosolic Ca concentration
  • divalent cation
  • rabbit platelets

ASJC Scopus subject areas

  • Pharmacology


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