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Inositol 1,4,5‐trisphosphate (IB 3 ) induced rapid formation of thromboxane B 2 in saponin‐permeabilised human platelets: mechanism of IP 3 action
Author(s) -
Authi Kalwant S.,
Hornby E.J.,
Evenden B.J.,
Crawford N.
Publication year - 1987
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(87)81471-0
Subject(s) - thromboxane , chemistry , saponin , egta , platelet activation , phospholipase c , inositol , phospholipase , intracellular , platelet , mechanism of action , biophysics , thromboxane a2 , antagonist , biochemistry , receptor , calcium , medicine , biology , in vitro , enzyme , alternative medicine , organic chemistry , pathology
The mechanism of IP 3 ‐induced activation of saponin‐permeabilised platelets has been examined. Saponin permeabilisation resulted in the leakage of low‐ M r substances into and from the cells without loss of cytoplasmic proteins. Addition of IP 3 rapidly induced a dose‐related formation of thromboxane B 2 and release into the medium, leading to the responses of shape change, aggregation and [ 14 C]5HT release. These responses were inhibited by the thromboxane A 2 receptor antagonist AH23848. The IP 3 ‐induced release of 4 Ca from intracellular stores was not affected by indomethacin. Synthesis of thromboxane was inhibited if Ca 2+ elevation was prevented by using Ca‐EGTA buffers during permeabilisation. These studies indicate that IP3‐induced activation was due to Ca 2+ mobilisation leading to phospholipase activation and thromboxane synthesis.