| pubmed-article:1432712 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1432712 | lifeskim:mentions | umls-concept:C0034493 | lld:lifeskim |
| pubmed-article:1432712 | lifeskim:mentions | umls-concept:C1519720 | lld:lifeskim |
| pubmed-article:1432712 | lifeskim:mentions | umls-concept:C0007277 | lld:lifeskim |
| pubmed-article:1432712 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
| pubmed-article:1432712 | lifeskim:mentions | umls-concept:C0205345 | lld:lifeskim |
| pubmed-article:1432712 | lifeskim:mentions | umls-concept:C1720920 | lld:lifeskim |
| pubmed-article:1432712 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:1432712 | pubmed:dateCreated | 1992-12-2 | lld:pubmed |
| pubmed-article:1432712 | 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) | lld:pubmed |
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| pubmed-article:1432712 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1432712 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1432712 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1432712 | pubmed:month | May | lld:pubmed |
| pubmed-article:1432712 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:1432712 | pubmed:author | pubmed-author:BiscoeT JTJ | lld:pubmed |
| pubmed-article:1432712 | pubmed:author | pubmed-author:DuchenM RMR | lld:pubmed |
| pubmed-article:1432712 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1432712 | pubmed:volume | 450 | lld:pubmed |
| pubmed-article:1432712 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1432712 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1432712 | pubmed:pagination | 33-61 | lld:pubmed |
| pubmed-article:1432712 | pubmed:dateRevised | 2010-9-7 | lld:pubmed |
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| pubmed-article:1432712 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1432712 | pubmed:articleTitle | Relative mitochondrial membrane potential and [Ca2+]i in type I cells isolated from the rabbit carotid body. | lld:pubmed |
| pubmed-article:1432712 | pubmed:affiliation | Department of Physiology, University College London. | lld:pubmed |
| pubmed-article:1432712 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1432712 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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