Open AccessOn the Interrelationship of Prostaglandin Endoperoxide G 2 and Cyclic Nucleotides in Platelet Function
Author(s) -
CLAESSON HansErik,
MALMSTEN Curt
Publication year - 1977
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1977.tb11593.x
Subject(s) - prostaglandin , chemistry , prostaglandin e1 , platelet , medicine , endocrinology , creatine kinase , nucleotide , prostaglandin e , adenosine , cyclic adenosine monophosphate , adenosine diphosphate , platelet aggregation , biochemistry , biology , receptor , gene
The prostaglandin endoperoxide G 2 caused rapid aggregation and release of ADP and [ 14 C]serotonin in human platelets. Since the presence of the ADP phosphorylating system creatine phosphate creatine phosphokinase markedly inhibited the aggregation caused by the endoperoxide, this effect seemed to be mediated mainly by ADP, which is instantaneously released by the endoperoxide. The prostaglandin G 2 counteracted the increasing effect of prostaglandin E 1 on the adenosine 3′:5′‐monophosphate (cAMP) levels in platelet‐rich plasma. This effect of prostaglandin G 2 was only observed when ADP was released by the endoperoxide. This finding indicates that the effect of prostaglandin G 2 on the cAMP levels in platelet‐rich plasma is principally mediated by ADP. The rapid release of ADP by prostaglandin G 2 and the time courses for the effects of the endoperoxide and ADP on the level of cAMP give further evidence for this hypothesis. ADP also caused primary aggregation in the presence of indomethacin, and prostaglandin synthesis inhibitors did not influence the decreasing effect of ADP on the cAMP levels. N 2 ,O 2 ‐Dibutyrylguanosine 3′:5′‐monophosphate did not influence the aggregation and release‐reaction caused by ADP and no changes of the cGMP levels were observed after addition of prostaglandin G 2 .