Fig. 6.
Thallium (Tl+) flux in cardiomyocytes and mitochondria from mice of varying Slo2 genotype. (A) Cardiomyocytes were isolated from wild-type (WT) (white bars) and Slo2.1−/− (black bars) mice, and surface K+ channel activity assayed via thallium (Tl+) uptake. Where indicated, isoflurane (Iso, 150 μM initial) and/or bepridil (Bep, 10 μM) were added. Data are normalized to control (no addition, dashed line) and are means ± SEM. 95% CIs are shown at top, number of replicates (N) at bottom, of each graph bar—see inset key in B. *Statistically significant difference versus control within a given genotype (ANOVA, with post hoc unpaired t test). (B) Mitochondria were isolated from WT (white bars), Slo2.x double knockout (dKO) (hashed), Slo2.1−/− (black), and Slo2.2−/− (gray) hearts, and K+ channel activity assayed via Tl+ uptake. Adenosine triphosphate (ATP) was present throughout to block mKATP channels. Where indicated, isoflurane (Iso, 300 μM initial) and/or bepridil (Bep, 10 μM) were added. Data are normalized to control (no addition) and are means ± SEM. 95% CIs are shown at top, number of replicates (N) at bottom, of each graph bar—see inset key. *Statistically significant difference versus ATP condition within a given genotype (ANOVA, with post hoc unpaired t test). (C) Cardiomyocyte Tl+ flux, as in A, but stimulated with bithionol (Bt, 0.25 μM) instead of isoflurane. Data are normalized to control (no addition, dashed line) and are means ± SEM. 95% CIs and N as per inset key in B. *Statistically significant difference versus control within a given genotype (ANOVA, with post hoc unpaired t test). (D) Mitochondrial Tl+ flux as in B but stimulated with bithionol (Bt, 2.5 μM) instead of isoflurane. Data are normalized to control (no addition) and are means ± SEM. 95% CIs and N as per inset key in B. *Statistically significant difference versus ATP condition within a given genotype (ANOVA, with post hoc unpaired t test). DZX = diazoxide.

Thallium (Tl+) flux in cardiomyocytes and mitochondria from mice of varying Slo2 genotype. (A) Cardiomyocytes were isolated from wild-type (WT) (white bars) and Slo2.1−/− (black bars) mice, and surface K+ channel activity assayed via thallium (Tl+) uptake. Where indicated, isoflurane (Iso, 150 μM initial) and/or bepridil (Bep, 10 μM) were added. Data are normalized to control (no addition, dashed line) and are means ± SEM. 95% CIs are shown at top, number of replicates (N) at bottom, of each graph bar—see inset key in B. *Statistically significant difference versus control within a given genotype (ANOVA, with post hoc unpaired t test). (B) Mitochondria were isolated from WT (white bars), Slo2.x double knockout (dKO) (hashed), Slo2.1−/− (black), and Slo2.2−/− (gray) hearts, and K+ channel activity assayed via Tl+ uptake. Adenosine triphosphate (ATP) was present throughout to block mKATP channels. Where indicated, isoflurane (Iso, 300 μM initial) and/or bepridil (Bep, 10 μM) were added. Data are normalized to control (no addition) and are means ± SEM. 95% CIs are shown at top, number of replicates (N) at bottom, of each graph bar—see inset key. *Statistically significant difference versus ATP condition within a given genotype (ANOVA, with post hoc unpaired t test). (C) Cardiomyocyte Tl+ flux, as in A, but stimulated with bithionol (Bt, 0.25 μM) instead of isoflurane. Data are normalized to control (no addition, dashed line) and are means ± SEM. 95% CIs and N as per inset key in B. *Statistically significant difference versus control within a given genotype (ANOVA, with post hoc unpaired t test). (D) Mitochondrial Tl+ flux as in B but stimulated with bithionol (Bt, 2.5 μM) instead of isoflurane. Data are normalized to control (no addition) and are means ± SEM. 95% CIs and N as per inset key in B. *Statistically significant difference versus ATP condition within a given genotype (ANOVA, with post hoc unpaired t test). DZX = diazoxide.

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