Potentiation with epinephrine of macaque platelet aggregation by other agonists: implications for studies on human atherosclerosis.

The effects of low concentrations of epinephrine on the aggregation of macaque and human platelets by arachidonic acid (AA), collagen, and thrombin were studied. When epinephrine (0.05 to 1 microM) was added to macaque or human citrated or macaque heparinized platelets, either before or after the addition of near-threshold concentrations of AA, significant increases in aggregability were always seen. Epinephrine alone did not aggregate macaque platelets from citrated blood. When near-threshold concentrations of collagen or thrombin were present in the medium, low concentrations of epinephrine (0.05 to 0.50 microM) potentiated the aggregation of macaque and human citrated platelets and macaque heparinized platelets. The P values for the addition of epinephrine were less than 0.01 in all series. The ability of low epinephrine concentrations to potentiate aggregation of macaque platelets by other agonists is of particular significance because in humans the most important effect of epinephrine on platelets in vivo is probably the potentiation, by low concentrations, of aggregation induced by other aggregatory agents normally present in the blood in low concentrations.