Hypoxia increases BK channel activity in the inner mitochondrial membrane.
To explore the potential function of the BK channel in the inner mitochondrial membrane under physiological and hypoxic conditions, we used on-mitoplast and whole-mitoplast patches. Single BK channels had a conductance of 276+/-9 pS under symmetrical K(+) solutions, were Ca(2+)- and voltage-dependent and were inhibited by 0.1 microM charybdotoxin. In response to hypoxia, BK increased open probability, shifted its reversal potential (9.3+/-2.4 mV) in the positive direction and did not change its conductance. We conclude that (1) the properties at rest of this mitoplast K(+) channel are similar to those of BK channels in the plasma membrane; (2) hypoxia induces an increase, rather than a decrease (as in the plasmalemma), in the open probability of this K(+) channel, leading to K(+) efflux from the mitochondrial matrix to the outside. We speculate that this increase in K(+) efflux from mitochondria into the cytosol is important during hypoxia in maintaining cytosolic K(+).
Gu
Xiang Q
XQ
Department of Pediatrics (Section of Respiratory Medicine), University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0735, USA.
Siemen
Detlef
D
Parvez
Suhel
S
Cheng
Yu
Y
Xue
Jin
J
Zhou
Dan
D
Sun
Xiaolu
X
Jonas
Elizabeth A
EA
Haddad
Gabriel G
GG
D002118:Calcium / Q000378:metabolism*; D015687:Cell Hypoxia; D045744:Cell Line, Tumor; D018999:Charybdotoxin / Q000494:pharmacology; D006801:Humans; D015640:Ion Channel Gating; D051036:Large-Conductance Calcium-Activated Potassium Channels / Q000502:physiology*; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology; D051336:Mitochondrial Membranes / Q000187:drug effects / Q000502:physiology*; D009498:Neurotoxins / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism*
D051036:Large-Conductance Calcium-Activated Potassium Channels; D009498:Neurotoxins; D018999:Charybdotoxin; D011188:Potassium; D002118:Calcium