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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
|
pubmed:dateCreated |
1993-12-17
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pubmed:abstractText |
The concentration of extracellular calcium rightly regulates calcitonin secretion by calcium influx through dihydropyridine-sensitive voltage-dependent calcium channels; the result is an increase in intracellular calcium. There also exists a cAMP-dependent pathway of calcitonin release activated by glucagon or growth hormone releasing hormone. In thyroid C-cells, as in all cells, there is dual regulation of adenylate cyclase, mediated by inhibitory or stimulatory G proteins; glucagon stimulated cAMP production can be inhibited by somatostatin via pertussis toxin sensitive inhibitory G proteins. Somatostatin inhibits not only cAMP dependent but also calcium-dependent calcitonin secretion. Furthermore, somatostatin inhibits voltage dependent calcium channel currents thereby lowering cytosolic calcium. These actions also involve a pertussis toxin-sensitive inhibitory G protein but they occur independently of changes in the cytosolic cAMP concentration. Thus multiple interactions between second messenger systems at different cellular levels modulate calcitonin secretion.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Sep
|
pubmed:issn |
0018-5043
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
25
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
473-6
|
pubmed:dateRevised |
2009-2-19
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pubmed:meshHeading | |
pubmed:year |
1993
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pubmed:articleTitle |
Regulation of calcitonin secretion in vitro.
|
pubmed:affiliation |
Abt. Innere Medizin I, Endokrinologie und Stoffwechsel, Universität Heidelberg, Germany.
|
pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
|