cAMP determinations alone may not detect activation or inhibition of the cAMP-PKA pathway, suggesting cAMP might still be an important second messenger for ADP-induced platelet aggregation.
cAMP assays may miss PKA pathway modulation in platelets; leaves open its role in ADP aggregation.
In rat platelets, basal cAMP levels were not changed upon stimulation with ADP and it was concluded that cAMP is not an important messenger for ADP-induced aggregation (Savi et al., Blood Coagul Fibrinolysis, 1996; 7: 249-52). In the present study, the effects of prostaglandin E(1) (PGE(1)) and ADP on human platelet aggregation, cAMP generation and VASP phosphorylation were studied. Phosphorylation of the protein kinase A (PKA) substrate VASP and inhibition of platelet aggregation by PGE(1) occurred without measurable changes in cellular cAMP levels. In addition, a marked inhibition of basal VASP phosphorylation by ADP was observed. It is concluded that cAMP determinations do not necessarily detect a possible activation or inhibition of the cAMPPKA pathway in platelets. Thus, cAMP might well be an important second messenger for ADP-induced platelet aggregation.
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Thomas Hohlfeld Artur-Aron Weber (1999) studied this question.
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