TY - JOUR
T1 - Ca2+‐dependent aggregation of rabbit platelets induced by maitotoxin, a potent marine toxin, isolated from a dinoflagellate
AU - Watanabe, Akiko
AU - Ishida, Yukisato
AU - Honda, Hiromi
AU - Kobayashi, Masaki
AU - Ohizumi, Yasushi
PY - 1993/5
Y1 - 1993/5
N2 - 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
AB - 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
KW - Maitotoxin
KW - aggregation
KW - cytosolic Ca concentration
KW - divalent cation
KW - rabbit platelets
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U2 - 10.1111/j.1476-5381.1993.tb13527.x
DO - 10.1111/j.1476-5381.1993.tb13527.x
M3 - Article
C2 - 8495244
AN - SCOPUS:0027536154
VL - 109
SP - 29
EP - 36
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
SN - 0007-1188
IS - 1
ER -