Skip to main content
. 2006 Jun 22;575(Pt 2):627–644. doi: 10.1113/jphysiol.2006.113985

Figure 9. Effects of 11,12-EET on cardiac KATP channels are not inhibited by PKI.

Figure 9

Recordings of HMR-1098-sensitive cardiac KATP currents in rat cardiac myocytes after treatment with 5 μm myristoylated PKI amide, showing the effects of extracellularly applied (A) and intracellular applied (B) 11,12-EET (5 μm). Pretreatment with myristoylated PKI amide had no effects on cardiac KATP channel sensitivity to 11,12-EET. C, cardiac KATP channel I–V relationships with no EET treatment (○), and with 11,12-EET applied extracellularly (▪) or intracellularly (•). n = 5 for all groups; *P < 0.05, intracellularly applied 11,12-EET versus baseline; †P < 0.05, extracellular 11,12-EET versus baseline; ‡P < 0.05, intracellular application versus extracellular application. D, recordings of glyburide-sensitive vascular KATP currents in rat mesenteric smooth muscle cells after treatment with 5 μm myristoylated PKI amide showing that the effects of extracellularly applied 11,12-EET were significantly attenuated. E, vascular KATP channel I–V relationship after treatment with PKI at baseline (□) and after exposure to 11,12-EET (▪). The effects of 11,12-EET were significantly inhibited by PKI (compare with Fig. 8D). n = 5; *P < 0.05, effect of 11,12-EET versus baseline. F, bar graphs comparing the percentage KATP current increase in cardiac myocytes (left panel) and vascular smooth muscle cells (right panel) by 11,12-EET applied intracellularly and extracellularly with and without (control) treatment with PKI. Group data showing the cardiac and vascular KATP current densities measured at −100 mV. Incubation with PKI had no effects on the activation of cardiac KATP channels by 11,12-EET, but significantly inhibited that in vascular KATP channels.