| pubmed-article:2078572 | rdf:type | pubmed:Citation | lld:pubmed |
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| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C1383501 | lld:lifeskim |
| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C0521428 | lld:lifeskim |
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| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C0205171 | lld:lifeskim |
| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C0443172 | lld:lifeskim |
| pubmed-article:2078572 | lifeskim:mentions | umls-concept:C0449774 | lld:lifeskim |
| pubmed-article:2078572 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:2078572 | pubmed:dateCreated | 1991-5-1 | lld:pubmed |
| pubmed-article:2078572 | pubmed:abstractText | The patterns of agonist-induced elevations of cytosolic free Ca2+ ([Ca2+]i) were characterized and compared by the use of single adrenal chromaffin cells. Initial histamine- or angiotensin II (AII)-induced elevations of [Ca2+]i were equal in magnitude (peaks 329 +/- 20 [SE] and 338 +/- 46 nM, respectively). These initial increases of [Ca2+]i were transient, insensitive to either Gd3+ or removing external Ca2+, and were primarily the result of Ca2+ release from intracellular stores. After the initial peak(s) of [Ca2+]i, a second phase of moderately elevated [Ca2+]i was observed, and this response was sensitive to either Gd3+ or removing external Ca2+, supporting a role for Ca2+ entry. In most cases, the second phase of elevated [Ca2+]i was sustained during histamine stimulation but transient during AII stimulation. Maintenance of the second phase was a property of the agonist rather than of the particular cell being stimulated. Thus, individual cells exposed sequentially to histamine and AII displayed distinct patterns of [Ca2+]i changes to each agonist, regardless of the order of addition. Histamine also stimulated twice as much [3H]catecholamine release as AII, and release was completely dependent on external Ca2+. Therefore, the ability of histamine and AII to sustain (or promote) Ca2+ entry appears to underlie their efficacy as secretagogues. These data provide evidence linking agonist-dependent patterns of [Ca2+]i changes in single cells with agonist-dependent functional responses. | lld:pubmed |
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| pubmed-article:2078572 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2078572 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2078572 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2078572 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2078572 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:2078572 | pubmed:issn | 1044-2030 | lld:pubmed |
| pubmed-article:2078572 | pubmed:author | pubmed-author:PrussR MRM | lld:pubmed |
| pubmed-article:2078572 | pubmed:author | pubmed-author:StaudermanK... | lld:pubmed |
| pubmed-article:2078572 | pubmed:author | pubmed-author:MurawskyM MMM | lld:pubmed |
| pubmed-article:2078572 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2078572 | pubmed:volume | 1 | lld:pubmed |
| pubmed-article:2078572 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2078572 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2078572 | pubmed:pagination | 683-91 | lld:pubmed |
| pubmed-article:2078572 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2078572 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2078572 | pubmed:articleTitle | Agonist-dependent patterns of cytosolic Ca2+ changes in single bovine adrenal chromaffin cells: relationship to catecholamine release. | lld:pubmed |
| pubmed-article:2078572 | pubmed:affiliation | Merrell Dow Research Institute, Cincinnati, Ohio 45215. | lld:pubmed |
| pubmed-article:2078572 | pubmed:publicationType | Journal Article | lld:pubmed |
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