Involvement of K+ movements in the membrane signal induced by PAF-acether.

We investigated the effects of PAF-acether and its specific antagonist BN 52021 on Na+ and K+ transport systems in human red cells and mouse macrophages. PAF-acether and BN 52021 exhibited specific and opposite effects on a Cs+-stimulated, K+ efflux in human red cells. PAF-acether increased and BN 52021 decreased the apparent dissociation constant for external Cs+ without significant effects on the maximal rate of K+ translocation. In mouse macrophages, PAF-acether stimulated a quinidine-sensitive K+ efflux. In the presence of the Ca2+-ionophore A 23187, PAF-acether and BN 52021 showed opposite effects (stimulation and inhibition respectively). For most cells, membrane potential is dependent on K+-permeability. In addition, opening of potential-dependent Ca2+ channels appears to be associated with cell activation in several models. We thus propose that the specific interaction of PAF-acether with a K+:K+ exchange increases Ca2+ uptake through transitory changes in membrane potential. This in turn may lead to a more permanent membrane hyperpolarization through to opening of Ca2+ dependent, K+ channels.