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

Figure 10. Effects of 11,12-EET on cardiac KATP channels are not inhibited by MIBG.

Figure 10

Recordings of HMR-1098-sensitive KATP currents recorded in rat ventricular myocytes after incubation with 100 μm MIBG (60 min), showing the effects of extracellularly (A) and intracellularly (B) applied 11,12-EET (5 μm). Incubation with MIBG (60 min) did not alter the activation of cardiac KATP channels by 11,12-EET. C, cardiac KATP channel I–V relationships with no EET treatment (○), and with 11,12-EET (5 μm) applied extracellularly (▪) or intracellularly (•). n = 6 for all groups; *P < 0.05, intracellularly applied 11,12-EET versus baseline; †P < 0.05, extracellularly applied 11,12-EET versus baseline; ‡P < 0.05, intracellularly applied versus extracellularly applied 11,12-EET. D, recordings of glyburide-sensitive KATP currents in rat mesenteric smooth muscle cells after treatment with 100 μm MIBG. E, vascular KATP channel I–V relationships after treatment with MIBG at baseline (□) and after exposure to 11,12-EET (▪), showing that the effects of extracellularly applied 11,12-EET were abolished, n = 6. 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 treatment with MIBG. Group data showing the cardiac and vascular KATP current densities measured at −100 mV.