Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1993-12-17
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
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
473-6
pubmed:dateRevised
2009-2-19
pubmed:meshHeading
pubmed:year
1993
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