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By David R. Phillips

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1980) found that neither aspirin nor indomethacin had any effect on the arachidonate-induced stimulation of cGMP production. This apparent discrepancy may be due to the fact that Best 2 42 EVELYN MEI H U A N G A N D T H O M A S C. DETWILER et al. (1980) used washed platelets suspended in buffer, whereas the other groups worked with platelets in plasma. Thus while the absolute levels of arachidonate used were comparable, the effective concentration would be much lower in plasma, where much of the fatty acid binds to proteins.

There are also observations that lead to skepticism about even a limited second 2 2 1. S T I M U L U S - R E S P O N S E C O U P L I N G MECHANISMS 35 messenger role for prostanoids. Under conditions such that cyclooxygenase inhibitors affect platelet function, there is very little prostanoid synthesis. , 1977). Thus, it appears that platelet activation by a weak agonist, such as ADP, involves aggregation-mediated induction of partial secretion and slight prostanoid synthesis, both of which are inhibited by aspirin and other cyclooxygenase inhibitors.

There is no evidence of platelet activation when a change in polar­ ization is imposed by high concentrations of extracellular Κ (deplorization) or by the K ionophore valinomycin (hyperpolarization). In addition, platelets are normally activated by agonists when ionophores block changes in membrane potential (Maclntyre and Rink, 1982). , 1972; Freidhoff and Sonenberg, 1983). Thus, the data suggest that a change in membrane potential is neither necessary nor sufficient for platelet activation but that it may modulate the platelet sensitivity to some agonists.

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