Effect of forskolin on platelet deaggregation and cyclic AMP generation.
The diterpene, forskolin, induced a partial deaggregation of ADP- or collagen-aggregated human platelets in vitro. An increase in platelet cyclic AMP by forskolin was assumed to mediate the platelet deaggregation. PGE1 also deaggregated these platelets, and a combination of forskolin and PGE1 produced deaggregation greater than the maximum which could be obtained with each agent alone. A greater than additive effect was observed on the platelet cyclic AMP level in the presence of both forskolin and PGE1. No additive effect was observed in the phosphorylation of molecular weight (Mr) 21K polypeptide using forskolin (0.1 mmol/l) and PGE1 (5 mumol/l) suggesting that although cyclic AMP is responsible for the deaggregation process a mechanism other than phosphorylation through cyclic AMP-dependent protein kinase may be responsible for the effect of forskolin on platelet deaggregation.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000527:Alprostadil / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D005576:Colforsin / Q000494:pharmacology*; D003094:Collagen / Q000494:pharmacology; D000242:Cyclic AMP / Q000096:biosynthesis*; D004357:Drug Synergism; D011464:Epoprostenol / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D010766:Phosphorylation; D010974:Platelet Aggregation / Q000187:drug effects*; D011506:Proteins / Q000378:metabolism
D011506:Proteins; D005576:Colforsin; D000244:Adenosine Diphosphate; D003094:Collagen; D011464:Epoprostenol; D000242:Cyclic AMP; D000527:Alprostadil