cAMP is not an important messenger for ADP-induced platelet aggregation
Autor: | A.M. Pflieger, P Savi, Jean-Marc Herbert |
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Rok vydání: | 1996 |
Předmět: |
P2Y receptor
medicine.medical_specialty Platelet Aggregation Down-Regulation Prostacyclin Second Messenger Systems Adenylyl Cyclase Inhibitors Rats Sprague-Dawley Adenylyl cyclase chemistry.chemical_compound Downregulation and upregulation Internal medicine Cyclic AMP medicine Animals Platelet Adenine Hematology General Medicine Clopidogrel Rats Adenosine Diphosphate Endocrinology chemistry Second messenger system Female Rabbits Platelet Aggregation Inhibitors medicine.drug |
Zdroj: | Blood Coagulation & Fibrinolysis. 7:249-252 |
ISSN: | 0957-5235 |
DOI: | 10.1097/00001721-199603000-00035 |
Popis: | In rat platelets, basal cAMP level did not vary significantly during ADP-induced aggregation. In the same conditions, no variation in the cAMP content was observed in platelets from rats treated with clopidogrel, whereas ADP-induced aggregation was totally inhibited. ADP decreased cAMP level in control prostacyclin- or forskolin-stimulated platelets whereas, in treated platelets, adenylyl cyclase down-regulation was strongly inhibited. SQ 22536 (500 microM), an inhibitor of adenylyl cyclase, strongly reduced the cAMP content of both control and treated platelets but did not reverse the anti-aggregating activity of clopidogrel, showing that inhibition of ADP-induced adenylyl cyclase down-regulation in treated platelets was not responsible for the anti-aggregating effect of clopidogrel. Similar results were obtained in rabbit platelets. These results therefore demonstrate that cAMP is not an important second messenger for ADP-induced platelet aggregation and suggest that another activating pathway, linked to the low affinity ADP receptor present on the platelet surface might be involved in the aggregation process. |
Databáze: | OpenAIRE |
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