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. 2022 Apr 19;13:2051. doi: 10.1038/s41467-022-29745-z

Fig. 3. Modulation of coronary arterial myocyte IKv upon changes in intracellular pyridine nucleotide redox potential.

Fig. 3

Isolated coronary arterial myocytes were dialyzed with pyridine nucleotides at concentrations as indicated in Supplementary Table 2 for voltage-clamp recordings in the conventional whole-cell configuration. A, B Representative outward K+ currents (A) and IK densities (pA/pF; B) recorded in coronary arterial myocytes from wild type mice (129SvEv) in the presence of either oxidized or reduced pyridine nucleotide redox ratios. Recordings were performed in the absence (i.) and presence (ii.) of the Kv1 channel inhibitor psora-4 (500 nM). Representative psora-4-sensitive currents (i.e., total outward IK – psora-insensitive IK) and summarized densities (mean values ± SEM) are shown in iii. panels. n = 5–6 cells, 4–5 mice for each. *P < 0.001, oxidized vs. reduced (mixed effects analysis). C Summarized I/Imax (mean values ± SEM) from two-pulse activation voltage protocol (i.) and inactivation protocol (ii.) for coronary arterial myocytes from wild type mice in the presence of oxidized or reduced pyridine nucleotide ratios. Curves were fit with a Boltzmann function; V0.5,act and V0.5,inact are provided in Supplementary Table 3. n = 5–6 cells, 4–5 mice for each. D Representative total outward IK and summarized IK density (mean values ± SEM), as in A, recorded in coronary arterial myocytes from Kvβ2−/− mice in the presence of either oxidized or reduced pyridine nucleotide ratios. n = 8–9 cells, 5 mice for each. (E) Plots showing summarized I/Imax (mean values ± SEM) with Boltzmann fittings, as in (D), recorded from coronary arterial myocytes from Kvβ2−/− mice. V0.5,act and V0.5,inact for each condition are provided in Supplementary Table 3. n = 5–7 cells, 4–5 mice for each. Source data are provided as a Source Data file.