Supplementary Figure 2: K_IR currents in pial artery SM cells were unaffected by knockout of K_IR2.1 in ECs.

(A) Typical experiment in a WT pial artery SM cell in which control currents (black trace) are characterized by an inwardly rectifying current at potentials negative to E_K (-23 mV) and an outwardly rectifying component at positive potentials. Application of 100 μM Ba²⁺ inhibited the inward rectifier component (red). Currents were recorded in response to a 200-ms ramp from -140 to +50 mV with 60 mM [K⁺]_o and 300 nM [Ca²⁺]_i. (B) Typical experiment in a pial artery SM cell from an EC K_IR2.1^−/− mouse under the same conditions. Ba²⁺ (blue trace) inhibited the inward rectifier component that was evident under control conditions (black trace). (C) Summary data at -140 mV, indicating no difference in SM cell K_IR current density between WT and EC K_IR2.1^−/− mice (WT, n = 14 cells from 3 mice; EC K_IR2.1^−/−, n = 13 cells from 4 mice; P = 0.5176 (t₂₅ = 0.6564) Student’s unpaired t-test). (D) The density of voltage-dependent currents at +50 mV was also unchanged between SM cells from WT and EC K_IR2.1^−/− mice (WT, n = 14 cells from 3 mice; EC K_IR2.1^−/−, n = 13 cells from 4 mice; P = 0.2002 (t₂₅ = 1.316) Student’s unpaired t-test). All error bars represent s.e.m.