We previously showed that in rat cardiomyocytes two types of mitoBKCa are present with high and low Po (∼0.85 and ∼0.01, respectively, at −60 mV in 12 µM Ca2+). We hypothesized that this difference could be related to the association with regulatory subunits. As first step, we investigated the role of BKCa β1 subunit by characterizing cardiac mitoBKCa properties in wild type (wt) and β1 KO mice. In wt mice, mitoBKCa was frequently recorded (in 6 out of 7 patches and 3 different preparations), had a conductance of ∼313 ± 8 pS (n=4) resembling that of mitoBKCa channel from rat (∼305 ± 19 pS, n=7), and was Ca2+ (n=2) and paxilline sensitive (n=3). In contrast to rat, wt mice had predominantly one population of mitoBKCa with a high open probability (Po∼0.8) at all membrane potentials tested (−80 to +80 mV, in 12 µM Ca2+). Interestingly, while in wt mice mitoBKCa were frequently recorded, in β1 KO, mitoBKCa was recorded only in 5 out of 24 patches (n=5 preparations). This channel had a similar conductance as the wt channel but with a much lower Po (∼0.25 vs. ∼0.8 at +60 mV in 12 µM Ca2+). These results are consistent with the view that in cardiac mitochondria, mitoBKCa is forming a complex with its β1 subunit favoring mitoBKCa expression and a high channel activity. A contribution of alternative subunits to mitoBKCa targeting and function needs further investigation. Supported by NIH and AHA.
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