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. 2010 Jul 12;588(Pt 17):3255–3266. doi: 10.1113/jphysiol.2010.194779

Figure 1. The presence of caveolin-1 reduces whole-cell recombinant Kir6.1/SUR2B currents.

Figure 1

A and B, representative pinacidil-evoked whole-cell Kir6.1/SUR2B currents recorded at −60 mV in 140 mm K+ from caveolin-null HEK293 (A) or a HEK293 cell line stably expressing caveolin-1 (B). The vascular KATP channel activator pinacidil (10 μm) and the specific KATP channel blocker glibenclamide (10 μm) were applied as indicated. The arrow indicates the extracellular solution was changed from 6 mm to 140 mm K+ to increase the inward driving force for K+. C, mean amplitude of glibenclamide-sensitive current in experiments like those in A and B (means ±s.e.m., n= 6, 8 cells, *P < 0.05). D, mean amplitude of glibenclamide-sensitive current in caveolin-null HEK293 cells in response to inclusion of caveolin-1 scaffolding domain peptide (SDP; 10 μm) or a scrambled version of this peptide (10 μm) in the pipette-filling solution (means ±s.e.m., n= 12, 6, 4 cells, **P < 0.01; n.s., not significant). The caveolin-1 SDP or the scrambled version of this peptide was allowed to dialyse into the cell for 10 min prior to the start of recording. E, response of caveolin-null HEK293 cells (filled symbols) or HEK293 cell line stably expressing caveolin-1 (open symbols) to different concentrations of pinacidil (3–100 μm; means ±s.e.m., n= 4, 3 cells, not significant).