thromboxane-b2 and tetrafluoroaluminate

Addition of fluoroaluminate to human platelet suspension stimulated thromboxane synthesis and inositol-1,4,5-triphosphate formation in a time and dose dependent manner. Neomycin inhibited markedly fluoroaluminate induced inositol-1,4,5-triphosphate formation without significantly affecting thromboxane synthesis. Preincubation of platelets with PGE1, also inhibited significantly inositol-1,4,5-triphosphate formation with modest reduction of thromboxane synthesis. On the contrary, pretreatment of platelets with pertussis toxin inhibited fluoroaluminate stimulated thromboxane synthesis without affecting inositol-1,4,5-triphosphate formation. Similarly, preincubation of platelets with phorbol ester, PMA, inhibited markedly thromboxane synthesis with modest reduction of inositol-1,4,5-triphosphate formation. These results indicate that inositol-1,4,5-triphosphate formation and arachidonate release and thromboxane synthesis are controlled separately and are mediated by different G-proteins which are coupled to phospholipase C and phospholipase A2 respectively in platelets.

Topics: Aluminum; Aluminum Compounds; Arachidonic Acid; Arachidonic Acids; Blood Platelets; Dose-Response Relationship, Drug; Epoprostenol; Fluorides; Fluorine; GTP-Binding Proteins; Humans; Inositol 1,4,5-Trisphosphate; Inositol Phosphates; Neomycin; Pertussis Toxin; Sodium Fluoride; Sugar Phosphates; Tetradecanoylphorbol Acetate; Thromboxane B2; Thromboxanes; Time Factors; Virulence Factors, Bordetella