cAMP reduces the affinity of Ca2+-triggered secretion in platelets.
Prostacyclin and other related compounds known to increase intracellular cAMP levels inhibit platelet responses. The mechanisms involved are only partially known, especially those concerning the complex relations between Ca2+ and cAMP as opposite intracellular mediators. Here, we have investigated aggregation and secretion in quin2-loaded platelets under conditions in which Ca2+ and cAMP are the only intracellular mediators. Our results show that cAMP inhibits aggregation and secretion in ionophore-treated cell without modifying their intracellular Ca2+ levels. This result suggests that the inhibition takes place on some intracellular target for Ca2+.
D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D002118:Calcium / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000494:pharmacology*; D004987:Ethers / Q000494:pharmacology; D005089:Exocytosis / Q000187:drug effects*; D006801:Humans; D015759:Ionomycin; D010974:Platelet Aggregation / Q000187:drug effects; D012636:Secretory Rate / Q000187:drug effects
D004987:Ethers; D005576:Colforsin; D015759:Ionomycin; D000242:Cyclic AMP; D002118:Calcium