Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1992-12-2
pubmed:abstractText
1. In the accompanying paper (Duchen & Biscoe, 1992) we have described graded changes in autofluorescence derived from mitochondrial NAD(P)H in type I cells of the carotid body in response to changes of PO2 over a physiologically significant range. These observations suggest that mitochondrial function in these cells is unusually sensitive to oxygen and could play a role in oxygen sensing. We have now explored further the relationships between hypoxia, mitochondrial membrane potential (delta psi m) and [Ca2+]i. 2. The fluorescence of Rhodamine 123 (Rh 123) accumulated within mitochondria is quenched by delta psi m. Mitochondrial depolarization thus increases the fluorescence signal. Blockade of electron transport (CN-, anoxia, rotenone) and uncoupling agents (e.g. carbonyl cyanide p-trifluoromethoxy-phenylhydrazone; FCCP) increased fluorescence by up to 80-120%, while fluorescence was reduced by blockade of the F0 proton channel of the mitochondrial ATP synthase complex (oligomycin). 3. delta psi m depolarized rapidly with anoxia, and was usually completely dissipated within 1-2 min. The depolarization of delta psi m with anoxia (or CN-) and repolarization on reoxygenation both followed a time course well characterized as the sum of two exponential processes. Oligomycin (0.2-2 micrograms/ml) hyperpolarized delta psi m and abolished the slower components of both the depolarization with anoxia and of the subsequent repolarization. These data (i) illustrate the role of the F1-F0 ATP synthetase in slowing the rate of dissipation of delta psi m on cessation of electron transport, (ii) confirm blockade of the ATP synthetase by oligomycin at these concentrations, and (iii) indicate significant accumulation of intramitochondrial ADP during 1-2 min of anoxia. 4. Depolarization of delta psi m was graded with graded changes in PO2 below about 60 mmHg. The stimulus-response curves thus constructed strongly resemble those for [Ca2+]i and NAD(P)H with PO2. The change in delta psi m closely followed changes in PO2 with time. 5. The rate of rise of [Ca2+]i in response to anoxia is strongly temperature sensitive. The rate of depolarization of delta psi m with anoxia similarly increased at least two- to fivefold on warming from 22 to 36 degrees C. The change with FCCP was not significantly altered by temperature. 6. These data show that the mitochondrial membrane potential changes over a physiological range of PO2 values in type I cells. This contrasts with the behaviour in dissociated chromaffin cells and sensory neurons, in which no change was measurable until the PO2 fell close to zero.(ABSTRACT TRUNCATED AT 400 WORDS)
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-1432706, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2193540, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2231419, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-224819, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2391654, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2557439, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2607457, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2720379, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2737279, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2738574, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2830260, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2863864, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-2873836, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-3419588, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-3745149, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-3946618, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-4223457, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-4313870, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-4320585, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-4338562, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-4429666, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-5499750, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-6245926, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-6291930, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-6424656, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-6783667, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-6965798, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-7263450, http://linkedlifedata.com/resource/pubmed/commentcorrection/1432712-7274216
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-3751
pubmed:author
pubmed:issnType
Print
pubmed:volume
450
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
33-61
pubmed:dateRevised
2010-9-7
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Relative mitochondrial membrane potential and [Ca2+]i in type I cells isolated from the rabbit carotid body.
pubmed:affiliation
Department of Physiology, University College London.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't