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

Fig. 4.

Fig. 4.

BK channel are involved in neurally evoked vasoconstriction in brain slices from SAH animals. (A) Simultaneous recordings of EFS-evoked changes in parenchymal arteriole diameter and astrocytic endfoot Ca2+ before and after incubation of SAH brain slices with HET0016 (HET; 100 nM), a blocker of CYP4A and 20-HETE synthesis. (B) Summary of the effects of HET0016 on EFS-evoked changes in arteriolar diameter and astrocytic endfoot Ca2+ obtained from SAH model rats (n = 6 brain slices from three animals). (C) Summary data demonstrating that the cyclooxygenase inhibitor, indomethacin (Indo; 10 μM) did not alter EFS-induced changes in diameter or endfoot Ca2+ in SAH model rats (n = 4 brain slices from two animals). (D) Simultaneous recordings of EFS-evoked changes in parenchymal arteriolar diameter and astrocytic endfoot Ca2+ before and after a 10-min incubation of brain slices with the BK channel blocker paxilline (Pax; 1 μM). (Scale bars, 10 μm.) (See also Movies S3 and S4.) (E) Summary data demonstrating that paxilline did not alter EFS-evoked changes in astrocytic endfoot Ca2+ but did greatly reduce EFS-induced constriction in SAH model rats (n = 5 brain slices from three animals). *P < 0.05 by Student’s t test. Error bars indicate SEM.