pubmed-article:3693357 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:3693357 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:3693357 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:3693357 | lifeskim:mentions | umls-concept:C0596030 | lld:lifeskim |
pubmed-article:3693357 | lifeskim:mentions | umls-concept:C0030580 | lld:lifeskim |
pubmed-article:3693357 | lifeskim:mentions | umls-concept:C1383501 | lld:lifeskim |
pubmed-article:3693357 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:3693357 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:3693357 | pubmed:issue | 36 | lld:pubmed |
pubmed-article:3693357 | pubmed:dateCreated | 1988-1-29 | lld:pubmed |
pubmed-article:3693357 | pubmed:abstractText | In order to analyze the factors regulating agonist-stimulated Ca2+ mobilization, cytosolic free [Ca2+] ([Ca2+]i) was measured directly in fura-2-loaded rat parotid acinar cells. Stimulation of muscarinic receptors by carbachol produced a dose-dependent rise in [Ca2+]i. In the presence of external Ca2+, the initial transient rise was followed by a maintained elevation. The maintained elevation is dependent on the presence of external Ca2+. Removal of Ca2+ by addition of EGTA caused a rapid decline in [Ca2+]i back to base line. In the absence of external Ca2+, only an initial transient peak in [Ca2+]i was seen which then declined to base line; the maintained elevation in [Ca2+]i could then be evoked by addition of Ca2+ in the continued presence of carbachol. Muscarinic receptor occupation by carbachol is required to maintain the elevated level of [Ca2+]i; addition of the muscarinic antagonist, atropine, caused [Ca2+]i to decline back to the basal level. The maintained elevation in [Ca2+]i, but not the initial transient peak, can also be blocked by Ni2+ but was unaffected by the organic Ca2+ antagonists. Total substitution of external Na+ with the impermeant cation, N-methyl-D-glucamine, had no effect on either the initial or the maintained response to carbachol; however, total substitution of Na+ with K+ attenuated the maintained response while not affecting the initial peak. Refilling of the intracellular Ca2+ store was also studied and found to take place in the absence of agonist and with no substantial elevation in [Ca2+]i. These experiments also showed that not all of the intracellular vesicular Ca2+ stores can be released by agonists. From these results, we propose a model for the regulation of [Ca2+]i. | lld:pubmed |
pubmed-article:3693357 | pubmed:language | eng | lld:pubmed |
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pubmed-article:3693357 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:3693357 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:3693357 | pubmed:month | Dec | lld:pubmed |
pubmed-article:3693357 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:3693357 | pubmed:author | pubmed-author:RinkT JTJ | lld:pubmed |
pubmed-article:3693357 | pubmed:author | pubmed-author:MerrittJ EJE | lld:pubmed |
pubmed-article:3693357 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:3693357 | pubmed:day | 25 | lld:pubmed |
pubmed-article:3693357 | pubmed:volume | 262 | lld:pubmed |
pubmed-article:3693357 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:3693357 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:3693357 | pubmed:pagination | 17362-9 | lld:pubmed |
pubmed-article:3693357 | pubmed:dateRevised | 2003-11-14 | lld:pubmed |
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pubmed-article:3693357 | pubmed:year | 1987 | lld:pubmed |
pubmed-article:3693357 | pubmed:articleTitle | Regulation of cytosolic free calcium in fura-2-loaded rat parotid acinar cells. | lld:pubmed |
pubmed-article:3693357 | pubmed:affiliation | Department of Cellular Pharmacology, Smith Kline and French Research Ltd., Welwyn, Herts, United Kingdom. | lld:pubmed |
pubmed-article:3693357 | pubmed:publicationType | Journal Article | lld:pubmed |
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