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Further Evidence for the Role of Thrombin in the Platelet Release Reaction Caused by Various Agents, and the Nature of Biphasic Platelet Aggregation
Author(s) -
Ardlie Neville G.
Publication year - 1978
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1978.tb01058.x
Subject(s) - chemistry , thrombin , egta , hirudin , heparin , platelet , calcium , epinephrine , chelation , biochemistry , platelet aggregation , adenosine diphosphate , biophysics , pharmacology , chromatography , medicine , inorganic chemistry , organic chemistry , biology
Studies were undertaken to resolve conflicting reports about the possible involvement of thrombin in the release reaction and second phase aggregation caused by ADP. Washed human platelets suspended in a buffered solution responded poorly to ADP, with no second phase aggregation or release of [ 3 H] 5 HT. In contrast, washed platelets suspended in dialysed plasma containing all intrinsic pathway clotting factors responded to ADP with second phase aggregation and release of radioactivity. This response depended on an optimum calcium concentration above which aggregation was impaired. Biphasic aggregation and release of platelet contents by ADP, epinephrine and collagen in dialysed plasma was inhibited by hirudin and heparin. The inhibitory effects of hirudin and heparin were not observed when citrate was present. These observations provide further evidence for the central role of thrombin in the release reaction and biphasic aggregation caused by various agents and indicate that these platelet reactions are not artifacts due to a citrate. Since the effect of citrate on aggregation and the inhibitory actions of hirudin and heparin were produced by another chelating agent, viz EGTA, it is suggested that the citrate effect is due to reduction of cation concentration.