The effects of somatostatin on the arachidonate cascade of platelets

Somatostatin (10(-9) M) significantly elevated the synthesis of thromboxane B2 in rat platelets. The transformation of arachidonic acid to active lipoxygenase metabolites was suppressed by somatostatin (10(-9) and 10(-8) M). The ratio of the lipoxygenase/cyclooxygenase products was significantly reduced by the polypeptide (10(-9) and 10(-8) M) in rat platelets. Higher concentrations (10(-7), 10(-6) and 10(-5) M) of somatostatin did not modify the lipoxygenase pathway of the platelets. The synthesis of the vasoconstrictor - proaggregatory cyclooxygenase products was stimulated by the polypeptide (10(-9) and 10(-8) M), while the formation of vasodilatator - antiaggregatory cyclooxygenase metabolites was induced by higher concentrations of somatostatin (10(-7) and 10(-6) M). Somatostatin might act on the deacylation process of phospholipids, reducing the free arachidonic acid substrate level, resulting in a lower lipoxygenation rate in the platelets, which could be responsible for the increased formation of thromboxane. The contradictory results reported by others concerning the action of somatostatin on the platelet function might be explained by our results that the effect of somatostatin depends on the applied dose.