| pubmed-article:8786359 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8786359 | lifeskim:mentions | umls-concept:C1179517 | lld:lifeskim |
| pubmed-article:8786359 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:8786359 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
| pubmed-article:8786359 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:8786359 | pubmed:dateCreated | 1996-9-26 | lld:pubmed |
| pubmed-article:8786359 | pubmed:abstractText | In a companion paper (Zhao, H., and S. Muallem. 1995), we describe the relationship between the major Na+,K+, and Cl- transporters in resting pancreatic acinar cells. The present study evaluated the role of the different transporters in regulating [Na+]i and electrolyte secretion during agonist stimulation. Cell stimulation increased [Na+]i and 86Rb influx in an agonist-specific manner. Ca(2+)-mobilizing agonists, such as carbachol and cholecystokinin, activated Na+ influx by a tetraethylammonium-sensitive channel and the Na+/H+ exchanger to rapidly increase [Na+]i from approximately 11.7 mM to between 34 and 39 mM. As a consequence, the NaK2Cl cotransporter was largely inhibited and the activity of the Na+ pump increased to mediate most of the 86Rb(K+) uptake into the cells. Secretin, which increases cAMP, activated the NaK2Cl cotransporter and the Na+/H+ exchanger to slowly increase [Na+]i from approximately 11.7 mM to an average of 24.6 mM. Accordingly, secretin increased total 86Rb uptake more than the Ca(2+)-mobilizing agonists and the apparent coupling between the NaK2Cl cotransport and the Na+ pump. All the effects of secretin could be attributed to an increase in cAMP, since forskolin affected [Na+]i and 86Rb fluxes similar to secretin. The signaling pathways mediating the effects of the Ca(2+)-mobilizing agonists were less clear. Although an increase in [Ca2+]i was required, it was not sufficient to account for the effect of the agonists. Activation of protein kinase C stimulated the NaK2Cl cotransporter to increase [Na+]i and 86Rb fluxes without preventing the inhibition of the cotransporter by Ca(2+)-mobilizing agonists. The effects of the agonists were not mediated by changes in cell volume, since cell swelling and shrinkage did not reproduce the effect of the agonists on [Na+]i and 86Rb fluxes. The overall findings of the relationships between the various Na+,K+, and Cl- transporters in resting and stimulated pancreatic acinar cells are discussed in terms of possible models of fluid and electrolyte secretion by these cells. | lld:pubmed |
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| pubmed-article:8786359 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8786359 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8786359 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8786359 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8786359 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:8786359 | pubmed:issn | 0022-1295 | lld:pubmed |
| pubmed-article:8786359 | pubmed:author | pubmed-author:MuallemSS | lld:pubmed |
| pubmed-article:8786359 | pubmed:author | pubmed-author:ZhaoHH | lld:pubmed |
| pubmed-article:8786359 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8786359 | pubmed:volume | 106 | lld:pubmed |
| pubmed-article:8786359 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8786359 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8786359 | pubmed:pagination | 1243-63 | lld:pubmed |
| pubmed-article:8786359 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8786359 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:8786359 | pubmed:articleTitle | Agonist-specific regulation of [Na+]i in pancreatic acinar cells. | lld:pubmed |
| pubmed-article:8786359 | pubmed:affiliation | Department of Physiology, University of Texas Southwestern Medical Center, Dallas 75235, USA. | lld:pubmed |
| pubmed-article:8786359 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8786359 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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