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Interaction between amitraz and alpha 2-adrenoceptors inhibits epinephrine-induced canine platelet aggregation.

The effect of amitraz, a formamidine insecticide, on [3H]yohimbine binding and aggregation of canine platelets was studied. The time course study of [3H]yohimbine binding to alpha 2-adrenoceptors on canine platelet membranes showed a maximum binding after 45 min at 37 degrees C using 5.25 nM final concentration of radioligand. When maximum binding was reached, amitraz (10(-4) M) was added to inhibit [3H]yohimbine binding. The dose-dependent inhibition of radioligand binding by amitraz was compared with that of chlordimeform, another formamidine insecticide, and clonidine. The IC50 values for clonidine, amitraz and chlordimeform indicated that amitraz was about 5 times less potent than clonidine and 6 times more potent than chlordimeform. Epinephrine (10(-6) M) promoted both primary and secondary aggregation of canine platelets in the presence of 10(-6) M ADP. Both amitraz (3 x 10(-7)-10(-5) M) and clonidine (3 x 10(-7)-10(-6) M) inhibited epinephrine-induced canine platelet aggregation in a dose-dependent manner. These results suggest that amitraz has a direct interaction with alpha 2-adrenoceptors of canine platelets to inhibit epinephrine-induced aggregation.