| pubmed-article:8057251 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8057251 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:8057251 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
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| pubmed-article:8057251 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:8057251 | lifeskim:mentions | umls-concept:C1519720 | lld:lifeskim |
| pubmed-article:8057251 | lifeskim:mentions | umls-concept:C0007277 | lld:lifeskim |
| pubmed-article:8057251 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
| pubmed-article:8057251 | lifeskim:mentions | umls-concept:C0025251 | lld:lifeskim |
| pubmed-article:8057251 | lifeskim:mentions | umls-concept:C0242184 | lld:lifeskim |
| pubmed-article:8057251 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:8057251 | lifeskim:mentions | umls-concept:C0037669 | lld:lifeskim |
| pubmed-article:8057251 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:8057251 | pubmed:dateCreated | 1994-9-15 | lld:pubmed |
| pubmed-article:8057251 | pubmed:abstractText | 1. We have studied the effects of hypoxia on membrane potential and [Ca2+]i in enzymically isolated type I cells of the neonatal rat carotid body (the principal respiratory O2 chemosensor). Isolated cells were maintained in short term culture (3-36 h) before use. [Ca2+]i was measured using the Ca(2+)-sensitive fluoroprobe indo-1. Indo-1 was loaded into cells using the esterified form indo-1 AM. Membrane potential was measured (and clamped) in single isolated type I cells using the perforated-patch (amphotericin B) whole-cell recording technique. 2. Graded reductions in PO2 from 160 Torr to 38, 19, 8, 5 and 0 Torr induced a graded rise of [Ca2+]i in both single and clumps of type I cells. 3. The rise of [Ca2+]i in response to anoxia was 98% inhibited by removal of external Ca2+ (+1 mM EGTA), indicating the probable involvement of Ca2+ influx from the external medium in mediating the anoxic [Ca2+]i response. 4. The L-type Ca2+ channel antagonist nicardipine (10 microM) inhibited the anoxic [Ca2+]i response by 67%, and the non-selective Ca2+ channel antagonist Ni2+ (2 mM) inhibited the response by 77%. 5. Under voltage recording conditions, anoxia induced a reversible membrane depolarization (or receptor potential) accompanied, in many cases, by trains of action potentials. These electrical events were coincident with a rapid rise of [Ca2+]i. When cells were voltage clamped close to their resting potential (-40 to -60 mV), the [Ca2+]i response to anoxia was greatly reduced and its onset was much slower.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
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| pubmed-article:8057251 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8057251 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8057251 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8057251 | pubmed:month | May | lld:pubmed |
| pubmed-article:8057251 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:8057251 | pubmed:author | pubmed-author:Vaughan-Jones... | lld:pubmed |
| pubmed-article:8057251 | pubmed:author | pubmed-author:BucklerK JKJ | lld:pubmed |
| pubmed-article:8057251 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8057251 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:8057251 | pubmed:volume | 476 | lld:pubmed |
| pubmed-article:8057251 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8057251 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8057251 | pubmed:pagination | 423-8 | lld:pubmed |
| pubmed-article:8057251 | pubmed:dateRevised | 2010-8-25 | lld:pubmed |
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| pubmed-article:8057251 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8057251 | pubmed:articleTitle | Effects of hypoxia on membrane potential and intracellular calcium in rat neonatal carotid body type I cells. | lld:pubmed |
| pubmed-article:8057251 | pubmed:affiliation | University Laboratory of Physiology, Oxford. | lld:pubmed |
| pubmed-article:8057251 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8057251 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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