Figure 9. Heparin does not interfere with the activation of I_CRAC by passive store depletion or with the effects of 2-APB.

In all experiments except as noted, 500 μg ml⁻¹ heparin was included in the recording pipette, and I_CRAC was induced through passive depletion of internal stores by 10 mm EGTA in the patch pipette. A and B, heparin affects neither the rate of I_CRAC activation (A) nor its maximal amplitude at steady state (B). The time to steady state was measured as the time to reach 95 % of the maximal current amplitude. Current amplitude was normalized to cell capacitance (average C_m= 9.95 pF). Heparin-treated cells (n = 6) are compared with matched control cells (n = 7). C, heparin loading via the patch pipette effectively inhibited IP₃ receptors. In control Jurkat cells lacking heparin, I_CRAC was activated by a 10 s UV flash to release caged IP₃ (15 μm). With 500 μg ml⁻¹ heparin in the pipette, uncaging IP₃ failed to activate I_CRAC. Results are representative of four cells loaded with caged IP₃ alone and three cells with caged IP₃ and heparin. D, 40 μm 2-APB first potentiated and then inhibited I_CRAC in a Jurkat cell loaded with heparin via the patch pipette. Shown here are the peak currents during steps to −100 mV from +30 mV. E, summary of the potentiating effects of 5 μm 2-APB in heparin-treated (n = 6) and matched control (n = 5) cells.