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Ca 2+ ‐dependent aggregation of rabbit platelets induced by maitotoxin, a potent marine toxin, isolated from a dinoflagellate
Author(s) -
Watanabe Akiko,
Ishida Yukisato,
Honda Hiromi,
Kobayashi Masaki,
Ohizumi Yasushi
Publication year - 1993
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1993.tb13527.x
Subject(s) - chemistry , verapamil , platelet , biophysics , calcium , thrombin , toxin , fura 2 , biochemistry , nifedipine , marine toxin , cytosol , pharmacology , medicine , enzyme , biology , organic chemistry
1 Administration of maitotoxin (MTX), a dinoflagellate toxin, caused aggregation of rabbit washed platelets. The cytosolic Ca 2+ concentration ([Ca 2+ ] i ), measured by fura‐2 fluorescence technique, was also increased by the presence of MTX. Rates of aggregation response and [Ca 2+ ] i ‐increase were dependent on tested concentrations (3–100 ng ml −1 ) of the toxin. 2 The MTX‐induced platelet aggregation and [Ca 2+ ] i ‐increase were totally abolished in a Ca 2+ ‐free solution. The successive administration of Ca 2+ in the presence of MTX elicited the aggregation and increase in [Ca 2+ ] i . 3 Ba 2+ was capable of substituting for Ca 2+ in the MTX‐induced platelet aggregation. In the presence of external Ca 2+ , transition metals, Co 2+ , Cd 2+ and Ni 2+ , inhibited the aggregation response to MTX. 4 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 m m ) reduced the rate of platelet aggregation. 5 MTX also elicited a release of ATP from platelets, which was abolished in the absence of external Ca 2+ . 6 In contrast, thrombin 0.5 unit ml −1 could elicit platelet shape change, [Ca 2+ ] i ‐increase and ATP‐release in the absence of external Ca 2+ . 7 These results suggest that the MTX‐induced platelet activation is caused by an enhanced Ca 2+ ‐influx presumably through voltage‐independent Ca 2+ channels on the plasma membrane.