In a mixed endoplasmic and surface-type membrane vesicle preparation from human platelets the polyphosphoinositides PIP and PIP2, similarly to IP3, were found to induce a rapid calcium release reaction. At physiological (resting) cytoplasmic calcium concentrations (0.1-0.3 μM) the PIP2 and IP3 concentrations producing half-maximum calcium release were similar (0.7 μM) and both agents could mobilize about 30-40% of the intravesicular calcium. However, the phosphodiesteric degradation of PIP2 in the membrane vesicles was found to be negligible and the ion- and drug-sensitivities of the calcium release reactions were different. The IP3-induced calcium release was selectively inhibited by micromolar calcium concentrations and by cinnarizine, while the PIP2-induced release was blocked by magnesium ions and neomycin. The calcium release evoked by either agent was inhibited by low concentrations of lanthanum but, in contrast to the ATP-dependent calcium pump, it was insensitive to vanadate, quercetin and to the lowering of the incubation temperature. When added simultaneously or in a rapid succession, maximum effective IP3 and PIP2 concentrations produced an additive calcium release reaction. Based on these data we suggest that IP3 and PIP2, respectively, induce rapid transmembrane calcium movements involving different transport pathways and/or membrane calcium pools, which are not related to the active calcium transport systems.
ASJC Scopus subject areas
- Cell Biology