CALCIUM STORE DEPLETION IN DIMETHYL BAPTA-LOADED HUMAN PLATELETS INCREASES PROTEIN-TYROSINE PHOSPHORYLATION IN THE ABSENCE OF A RISE IN CYTOSOLIC CALCIUM

The endomembrane Ca2+-ATPase inhibitor, thapsigargin, was used to depl ete the intracellular Ca2+ stores of fura-2-loaded human platelets. In control cells, thapsigargin evoked a rise in cytosolic [Ca2+] and a s ubstantial increase in protein tyrosine phosphorylation. Thapsigargin also evoked an increase in tyrosine phosphorylation in cells co-loaded with fura-2 and the Ca2+ chelator dimethyl BAPTA, such that the rise in cytosolic [Ca2+] was abolished. These data support the existence of a tyrosine phosphatase regulated by the Ca2+ content of the intracell ular store, a requirement of the putative model for reciprocal control of Ca2+ entry by cytosolic and store [Ca2+] via protein tyrosine phos phorylation.