Pyridoxal phosphate inhibition of platelet function.
The effect of pyridoxal phosphate (PLP) on human platelet function in vitro was studied. PLP inhibited adenosine diphosphate (ADP)-induced shape change, aggregation, and the potentiation by ADP of arachidonic acid-induced aggregation. This inhibition could easily be reversed by increasing concentrations of ADP or by removing PLP. The addition of sodium borohydride to PLP-treated platelets produced an irreversible inhibition of ADP aggregation. Thus it is possible that PLP inhibited ADP-induced platelet function by forming a Schiff base with platelet-surface amino groups. PLP also produced a partial inhibition of platelet aggregation to epinephrine, arachidonic acid, A23187, and a dose-dependent inhibition of [14C]serotonin release to epinephrine and arachidonic acid. PLP did not inhibit [14C]serotonin release to A23187, nor did it suppress arachidonic acid-induced malondialdehyde production. The conclusion is drawn that the partial inhibition by PLP of platelet aggregation observed to epinephrine, arachidonic acid, and A23187 resulted from PLP's inhibition of the effect of released ADP.
D000244:Adenosine Diphosphate / Q000378:metabolism; D001095:Arachidonic Acids / Q000378:metabolism; D001792:Blood Platelets / Q000378:metabolism / Q000502:physiology*; D001894:Borohydrides / Q000378:metabolism; D000001:Calcimycin / Q000494:pharmacology; D003864:Depression, Chemical; D004837:Epinephrine / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D008315:Malondialdehyde / Q000096:biosynthesis; D010974:Platelet Aggregation / Q000187:drug effects; D011732:Pyridoxal Phosphate / Q000494:pharmacology*; D012701:Serotonin / Q000378:metabolism
D001095:Arachidonic Acids; D001894:Borohydrides; D012701:Serotonin; D000001:Calcimycin; D008315:Malondialdehyde; D011732:Pyridoxal Phosphate; D000244:Adenosine Diphosphate; D004837:Epinephrine