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. 2010 Jan 15;588(Pt 2):283-6.
doi: 10.1113/jphysiol.2009.179028.

Mitochondrial ATP-sensitive K+ channels, protectors of the heart

Mitsuhiko Yamada  1
Affiliations

Mitochondrial ATP-sensitive K+ channels, protectors of the heart

Mitsuhiko Yamada. J Physiol. .
No abstract available

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Figures

Figure 1
Figure 1
Ion transporters on the mitochondrial inner membrane described in the text A horizontal grey bar indicates the mitochondrial inner membrane. This membrane is polarized by ∼180 mV with matrix side negative (ΔΨm) due to a H+ gradient generated by respiratory enzyme complexes (REC) (Bernardi, 1999; Saraste, 1999). The energy stored in the form of ΔΨm is utilized to make ATP from ADP by ATP synthetase (AS). Mitochondrial ATP-sensitive channels (mitoKATP) mediate K+ influx along ΔΨm and cause a decrease in ΔΨm, matrix swelling and regulation of reactive oxygen species (ROS) generation. MitoKATP channels are activated by K+ channel opener compounds (KCOs) and inhibited by ATP, glybenclamide (Glb) and 5-hydroxydecanoic acid (5-HD). A decrease in ΔΨm inhibits Ca2+ influx through Ca2+ unipoters (Ca2+UP). Ca2+UP is inhibited by ruthenium red (RR). Mitochondrial permeability transition pore (PTP) is a specific, voltage-dependent, non-selective high-conductance channel that is activated by an increase in the intra-mitochondrial Ca2+ concentration and a decrease in ΔΨm. Ca2+ efflux through PTP is also facilitated by a decrease in ΔΨm. PTP is inhibited by cyclosporin A (Cys A).
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