The Stimulation of human platelets by thrombin leads to the activation of phospholipases C and A2, protein kinases, formation of 3-inositol phos- pholipids and mobilization of Ca2+ . These biochemical reactions closely parallel platelet shape change, granular secretion and aggregation. The membrane-bound transducers for the thrombin receptor seem to be the heterotrimeric G protein G12 and the ras-related G protein rap 1-b. Phosphorylation of rap 1-b by the action of the cyclic AMP-dependent protein kinase seems to uncouple the thrombin receptor from phospholipases. This causes inhibition of the formation of second messenger molecules and the onset of physiological responses.