Linked Life Data

10209304

Source:http://linkedlifedata.com/resource/pubmed/id/10209304

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-5-25
pubmed:abstractText
Different signal transduction pathways, i.e. Ca2+- and cAMP-dependent, involved in mediating the effects of angiotensin II (AII) were investigated separately using the short-circuit current (Isc) technique and radioimmunoassay (RIA) in a cystic fibrosis pancreatic cell line (CFPAC-1) which exhibits defective cAMP-dependent but intact Ca2+-dependent anion secretion. The AII-induced Isc could be inhibited by the specific antagonist for AT1, losartan (1 microM), but not the antagonist for AT2, PD123177 (up to 10 microM). The AII-induced Isc was also reduced by the treatment of the cells with a Ca2+ chelator, BAPTA-AM (100 microM), indicating a dependence of the AII-induced anion secretion on the intracellular Ca2+. Treatment of the cells with pertussis toxin (0.1 microg/ml) or a phospholipase C (PLC) inhibitor, U73122 (5 microM), resulted in a substantial reduction in the AII-induced Isc indicating involvement of Gi and PLC in the Ca2+-dependent anion secretion. RIA measurements showed that AII stimulated an increase in cAMP production which could be reduced by losartan, pertussis toxin and U73122 but not BAPTA-AM. In addition, inhibitors of cyclooxygenase, indomethacin (10 microM) and piroxicam (10 microM), did not have any effect on the AII-induced cAMP production, excluding the involvement of prostaglandins. Our results suggest that both AII-stimulated cAMP and Ca2+-dependent responses are mediated by the AT1 receptor and Gi-coupled PLC pathway. However, the AII-stimulated cAMP production in CFPAC-1 cells is not dependent on Ca2+ or the formation of prostaglandins.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/1-(6-((3-methoxyestra-1,3,5(10)-trie..., http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II, http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP, http://linkedlifedata.com/resource/pubmed/chemical/Estrenes, http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin, http://linkedlifedata.com/resource/pubmed/chemical/Pyrrolidinones, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 2, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Angiotensin, http://linkedlifedata.com/resource/pubmed/chemical/Type C Phospholipases, http://linkedlifedata.com/resource/pubmed/chemical/Virulence Factors, Bordetella
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
1449
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
254-60
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Angiotensin II-mediated signal transduction events in cystic fibrosis pancreatic duct cells.
pubmed:affiliation
Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't