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. 2012 Apr 30;109(21):E1387–E1395. doi: 10.1073/pnas.1121359109

Fig. 5.

Fig. 5.

K+-induced dilations are absent in brain slices from SAH model animals despite the presence of functional smooth muscle Kir channels. (A) Elevation of K+ from 3 mM to 10 mM in aCSF superfusate dilated parenchymal arterioles in brain slices from control (n = 5 brain slices from two animals) but not in brain slices from SAH model (n = 5 brain slices from three animals) rats. (B) Brain slices were treated with the BK channel blocker paxilline (Pax; 1 μM) for 10 min before superfusion with aCSF containing 10 mM K+ and paxilline. Paxilline restored K+-induced dilations in brain slices from SAH model rats (n = 8 brain slices from four animals). K+-induced dilations were similar in the absence and presence of paxilline in brain slices from control animals (n = 7 brain slices from four animals). (C) Diameter changes obtained from isolated pressurized parenchymal arterioles from control (n = 4 arterioles from four animals) and SAH model (n = 3 arterioles from three animals) rats. Diameter changes are expressed relative to the initial diameter in aCSF containing 3 mM K+. (D) Ba2+-sensitive Kir currents measured in 140 mM extracellular K+ during 500-ms voltage ramps from −100 mV to +40 mV. (E) Summary data of current density recorded at −100 mV in parenchymal arteriolar myocytes isolated from control (n = 12 cells from three animals) and SAH (n = 9 cells from three animals) rats. *P < 0.05 by Student’s t test. Error bars indicate SEM.