Effects of ADP and Epinephrine on Macaque and human Platelets implications for studies on human atherosclerosis

Abstract

The ranges for near-threshold ADP concentrations for the aggregation of macaque and human citrated platelets overlapped. The minimum concentrations of epinephrine, 0.05 μM to 1.0 μM, that at least doubled the aggregation response at threshold ADP concentrations were comparable for macaque and human citrated platelets. Epinephrine (1.0 μM to 10 mM) alone never aggregated macaque citrated platelets. Biphasic aggregation occurred with both macaque and human citrated platelets. The addition of heparin to a final concentration of 2.2 units/ml had no effect on the threshold ADP concentrations or the sensitivity of macaque or human citrated platelets to epinephrine. One μM phentolamine eliminated the potentiating effect of 1 μM epinephrine on ADP-induced aggregation of macaque and human citrated platelets. The threshold concentrations of ADP for macaque platelets were sharply reduced when heparin was used as an anticoagulant rather than citrate. However, epinephrine induced a similar increase in aggregability with both citrated and heparinized platelets, 0.55 ± 0.09 SEM% and 0.44 ± 0.09 SEM%, respectively. These data indicate that macaque and human platelets behave in a similar manner in response to ADP and that epinephrine potentiates the ADP-induced aggregation of macaque and human platelets equally well.