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The time to current activation was unaffected by 100 M TMAO (Figures 10G,H), suggesting little modulation of this channel complex or, similar to data in Figure 4, alterations to ATP synthesis, given this channels role as an ATP sensor ( To determine whether activation of Kir6.1 in cardiomyocytes was responsible for the reduction in contractile efficacy identified in Figure 9, experiments were carried out in the presence of 10 M PNU37883A to inhibit the Kir6.1 current in ventricular myocytes in the presence of 100 M TMAO

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