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. 2012 Oct 4;7(10):e46865. doi: 10.1371/journal.pone.0046865

Figure 2. Pharmacological profiles of S2R+ IClswell and IdBest1 match and differ from those of HEK IClswell and Id64m.

Figure 2

(A–D) % Block of S2R+ IClswell, IdBest1, HEK IClswell and Id64m by 1 mM furosemide, 100 µM DIDS, and 30 µM DCPIB. Block at 0 mV is presented to emphasize the incomplete voltage-dependent DCPIB block of S2R+ IClswell and IdBest1. (A) Steady state S2R+ IClswell activated by 200 mOSM stimulation was blocked 96% ±1.6 by furosemide, 19% ±4 by DIDS, and 52% ±10.6 by DCPIB. * no difference compared to IdBest1 block and significantly different compared to HEK IClswell and Id64m (ANOVA, p<0.05). (B) IdBest1, stimulated for 2 min by 200 mOSM, was blocked 96% ±1.7 by furosemide, 44% ±10 by DIDS, and 47% ±10.9 by DCPIB. * no difference compared to S2R+ IClswell block and significantly different compared to HEK IClswell and Id64m (ANOVA, p<0.05). (C) Steady-state HEK IClswell activated by 200 mOSM stimulation was blocked 7% ±3.5 by furosemide, 77% ±3 by DIDS, and 99% ±0.7 by DCPIB. (D) Constitutive Id64m (320 mOSM) was blocked 77% ±3 by furosemide, 98% ±1.5 by DIDS, and 98% ±1.2 by DCPIB. Inline graphic significantly different compared to S2R+ IClswell, HEK IClswell and Id64m (ANOVA, p<0.05). (E–F) I–V relations for S2R+ IClswell and IdBest1 demonstrate DCPIB voltage-dependent block. At 80 mV, DCPIB block of S2R+ IClswell is 90% ±3.6 (n = 6), and 82% ±6.5 for IdBest1 (n = 7).