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- W1992926617 abstract "<h2>Abstract</h2> The mechanism by which low doses of epinephrine or ADP potentiate primary platelet aggregation was investigated. Aspirin (lmg/ml)-treated human blood platelets were isolated by albumin density gradient centrifugation. Platelet <sup>45</sup>Ca uptake associated with epinephrine or ADP addition was determined over a 240 sec time course. Pretreatment of the platelets with ADP (0.5μM) significantly increased aggregation in response to epinephrine (0.1μM). This increased aggregation was associated with a substantially greater <sup>45</sup>Ca uptake than that which occurred in the presence of epinephrine (0.1μM) alone. The potentiated epinephrine response was inhibited by the Ca<sup>2+</sup> antagonist verapamil (25μM). This inhibition could in turn be reduced by Ca<sup>2+</sup> (1mM) addition. Pretreatment of platelets with epinephrine (0.1μM) also increased aggregation in response to ADP (0.5μM). Although this potentiated response was not associated with measurable <sup>45</sup>Ca uptake, it was nevertheless completely abolished by verapamil (25μM) treatment. These findings suggest that low doses of ADP promote the ability of epinephrine to stimulate an increase in membrane permeability to Ca<sup>2+</sup>." @default.
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- W1992926617 date "1980-03-01" @default.
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- W1992926617 title "The involvement of calcium in epinephrine or ADP potentiation of human platelet aggregation" @default.
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- W1992926617 doi "https://doi.org/10.1016/0049-3848(80)90250-9" @default.
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