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. 2011 Aug 12;301(5):L745–L754. doi: 10.1152/ajplung.00020.2011

Fig. 4.

Fig. 4.

PKCβ mediates enhanced vasoconstrictor reactivity to ET-1 following E-IH. Vasoconstrictor (A, C, E, G) and VSM [Ca2+]i (B, D, F, H) responses to ET-1 in the presence and absence of the general PKC antagonist Ro 31-8220 (5 μmol/l) (A and B), the PKCδ antagonist rottlerin (3 μmol/l) (C and D), the selective PKCα/β inhibitor myr-PKC (10 μmol/l) (E and F), or the selective PKCβ inhibitor LY-333-531 (10 nmol/l) (G and H). Data are means ± SE of n = 4–9/group. *P < 0.05 E-IH vs. sham; #P < 0.05 E-IH vs. E-IH + drug; †P < 0.05 sham vs. sham + drug, ‡P < 0.05 E-IH + drug vs. sham + drug.