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The release of nucleotides, 5‐hydroxytryptamine and enzymes from human blood platelets during aggregation
Author(s) -
Mills D. C. B.,
Robb I. A.,
Roberts G. C. K.
Publication year - 1968
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1968.sp008484
Subject(s) - chemistry , adenylate kinase , platelet , adenosine diphosphate , degranulation , adenine nucleotide , enzyme , biochemistry , nucleotide , adenosine monophosphate , thrombin , platelet aggregation , phosphatase , adenosine , acid phosphatase , medicine , receptor , gene
1. Adenosine diphosphate (ADP) and adrenaline caused the aggregation of human platelets suspended in plasma containing citrate anticoagulant and stirred at 37° C. The aggregation occurred in two phases and the second phase was associated with the appearance in the plasma of up to 30% of the ATP and 55% of the ADP present in the platelets. The concentration of ADP appearing in the plasma was up to 7 times the concentration added. 2. Radioactivity was released by ADP and by adrenaline from platelets labelled with radioactive 5‐hydroxytryptamine; this release was closely correlated with the second phase of aggregation and with the release of nucleotides. 3. Acid phosphatase, β‐glucuronidase and adenylate kinase were released to a small extent during second phase aggregation by ADP or adrenaline; thrombin and collagen particles caused significantly greater release of β‐glucuronidase than of either acid phosphatase or of adenylate kinase. 4. Morphological changes indicating degranulation of the platelets were observed during the second phase of aggregation produced by adrenaline and by ADP. 5. The second phase of aggregation, degranulation of platelets, and the release of nucleotides, of labelled 5‐hydroxytryptamine and of enzymes, were all inhibited by concentrations of amitriptyline which did not inhibit aggregation.