Figure 1. Effects of AA metabolites on cardiac K_ATP channel activities in rat ventricular myocytes.

A, whole-cell total K⁺ currents were elicited from −120 mV to +20 mV at a holding potential of 0 mV at increments of 10 mV in control rat ventricular myocytes. K⁺ currents were activated by 1 μm AA, reaching steady state in 10 min, and then exposed to 3 μm HMR-1098. B, I–V relationships of total K⁺ currents at baseline, in response to 1 μm AA, and 3 μm HMR-1098. C, HMR-1098-sensitive K⁺ currents (cardiac K_ATP currents) were obtained from the current tracings in A by digital subtraction of the residual currents after exposure to HMR-1098 (3 μm) from the total K⁺ currents. K_ATP currents were activated by AA. D, the K_ATP channel I–V relationships show inward rectification with a reversal potential of −70 mV. AA (1 μm) enhanced K_ATP currents at all voltages negative to reversal potential (inward currents). Treatment with 10 μm miconazole reduced K_ATP current densities at baseline and abolished the response to AA. Each point represents the mean ± s.e.m. ^*P < 0.05 for AA versus baseline (n = 6). †P < 0.05 for baseline currents with versus without miconazole treatment (n = 5).