Article date: May 1993
By: Akiko Watanabe, Yukisato Ishida, Hiromi Honda, Masaki Kobayashi, Yasushi Ohizumi, in Volume 109, Issue 1, pages 29-36
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 (10−5m) 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.
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 (10−5m) 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.
DOI: 10.1111/j.1476-5381.1993.tb13527.x
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