Evidence for the receptor-operated calcium channels in human platelet plasma membrane.
Loading of human platelets with quin2 considerably increases platelet activating factor (PAF)-induced 45Ca2+ uptake. 45Ca2+ binding in the absence of agonists remains unchanged. The data show that PAF stimulates calcium ion influx into platelets, since quin2 provides substantial additional buffer capacity for Ca2+ in the cytoplasm. PAF and prostaglandin endoperoxide H2 analogue, U46619, induce Ba2+ and Mn2+ entry. The entrance of these cations and the rise in [Ca2+]i are both blocked by cAMP elevation and activation of protein kinase C by phorbol ester which indicates a single mechanism for agonist-induced transport of all three cations into platelets. It is assumed that agonists stimulate Ca2+ entry through the receptor-operated channels.
D000527:Alprostadil / Q000494:pharmacology; D000634:Aminoquinolines; D001464:Barium / Q000494:pharmacology; D001692:Biological Transport; D001792:Blood Platelets / Q000502:physiology*; D002118:Calcium / Q000097:blood*; D002462:Cell Membrane / Q000502:physiology; D006801:Humans; D066298:In Vitro Techniques; D007473:Ion Channels / Q000502:physiology*; D010972:Platelet Activating Factor / Q000494:pharmacology; D011956:Receptors, Cell Surface / Q000502:physiology*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D000634:Aminoquinolines; D007473:Ion Channels; D010972:Platelet Activating Factor; D011956:Receptors, Cell Surface; D001464:Barium; C035738:Quin2-acetoxymethyl ester; D000527:Alprostadil; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium