Increase of empty pool-activated Ca2+ influx using an intracellular Ca2+ chelating agent

We demonstrate here that stimulated 45Ca2+ influx in A7r5 vascular smooth muscle cells induced either by receptor activation with Arg]8 vasopressin or by the SR-Ca(2+)-ATPase inhibitor thapsigargin was increased more than threefold if cells were preloaded with the intracellular calcium chelator BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid). The increased influx is probably due to an attenuation of negative feedback of Ca2+ on its own entry accompanied by increased Ca2+ storage capacity of BAPTA-loaded cells leading to diminished cellular Ca2+ release. We propose that BAPTA preloading could be a useful approach to investigate receptor-induced Ca2+ influx.