Source:http://linkedlifedata.com/resource/pubmed/id/15345496
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2004-9-3
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pubmed:abstractText |
We investigated the involvement of intracellular and extracellular Ca2+ in the stimulation of Na+ transport during hyposmotic treatment of A6 renal epithelia. A sudden osmotic decrease elicits a biphasic stimulation of Na+ transport, recorded as increase in amiloride-sensitive short-circuit current (Isc) from 3.4 +/- 0.4 to 24.0 +/- 1.3 microA/cm2 (n = 6). Changes in intracellular Ca2+ concentration ([Ca2+]i) were prevented by blocking basolateral Ca2+ entry with Mg2+ and emptying the intracellular Ca2+ stores before the hyposmotic challenge. This treatment did not noticeably affect the hypotonicity-induced stimulation of Isc. However, the absence of extracellular Ca2+ severely attenuated Na+ transport stimulation by the hyposmotic shock, and Isc merely increased from 2.2 +/- 0.3 to 4.8 +/- 0.7 microA/cm2. Interestingly, several agonists of the Ca2+-sensing receptor, Mg2+ (2 mM), Gd3+ (0.1 mM), neomycin (0.1 mM), and spermine (1 mM) were able to substitute for extracellular Ca2+. When added to the basolateral solution, these agents restored the stimulatory effect of the hyposmotic solutions on Isc in the absence of extracellular Ca2+ to levels that were comparable to control conditions. None of the above-mentioned agonists induced a change in [Ca2+]i. Quinacrine, an inhibitor of PLA2, overruled the effect of the agonists on Na+ transport. In conclusion, we suggest that a Ca2+-sensing receptor in A6 epithelia mediates the stimulation of Na+ transport without the interference of changes in [Ca2+]i.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Hypotonic Solutions,
http://linkedlifedata.com/resource/pubmed/chemical/Magnesium,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipases A,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipases A2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Calcium-Sensing,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Water
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1931-857X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
287
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
F840-9
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pubmed:dateRevised |
2011-4-28
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pubmed:meshHeading |
pubmed-meshheading:15345496-Animals,
pubmed-meshheading:15345496-Calcium,
pubmed-meshheading:15345496-Cell Line,
pubmed-meshheading:15345496-Electric Conductivity,
pubmed-meshheading:15345496-Extracellular Space,
pubmed-meshheading:15345496-Hypotonic Solutions,
pubmed-meshheading:15345496-Magnesium,
pubmed-meshheading:15345496-Osmolar Concentration,
pubmed-meshheading:15345496-Osmotic Pressure,
pubmed-meshheading:15345496-Phospholipases A,
pubmed-meshheading:15345496-Phospholipases A2,
pubmed-meshheading:15345496-Receptors, Calcium-Sensing,
pubmed-meshheading:15345496-Signal Transduction,
pubmed-meshheading:15345496-Sodium,
pubmed-meshheading:15345496-Urothelium,
pubmed-meshheading:15345496-Water,
pubmed-meshheading:15345496-Xenopus laevis
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pubmed:year |
2004
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pubmed:articleTitle |
Extracellular Ca2+ regulates the stimulation of Na+ transport in A6 renal epithelia.
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pubmed:affiliation |
Laboratory of Physiology, Biomedical Research Institute, Limburgs Universitair Centrum, Universitaire Campus, B-3590 Diepenbeek, Belgium.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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