File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Angiotensin II evokes calcium-mediated signaling events in isolated dog pancreatic epithelial cells

TitleAngiotensin II evokes calcium-mediated signaling events in isolated dog pancreatic epithelial cells
Authors
KeywordsAngiotensin II
Calcium-mediated chloride channels
Pancreatic ductal secretion
Issue Date2002
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.pancreasjournal.com
Citation
Pancreas, 2002, v. 25 n. 3, p. 290-295 How to Cite?
AbstractIntroduction: Calcium-activated chloride conductance has been identified in normal pancreatic duct cells. Recent in vitro evidence suggests that angiotensin II (AngII) stimulates pancreatic secretion in both cystic fibrosis (CFPAC) and transformed pancreatic cells. Aims: To investigate calcium-mediated stimulatory effects of AngII in both nontransformed dog pancreatic duct epithelial (DPDE) and CFPAC cells. Methods: Western blots were performed in both cells seeking AngII receptors. In additional studies, DPDE and CFPAC cells were grown on vitrogen-coated glass cover slips and loaded with Indo-1-AM dye. Cells were placed in a confocal microscope's perfusion chamber and perfused with 100 μM AngII or ATP (control). Cells were excited with UV light, and intracellular calcium ([Ca+2]i) was read using fluorescence emission at 405 and 530 nm. Finally, single channels in the DPDE cells were examined using cell-attached patch clamps. Current amplitude histograms provided estimates of the conductance and open probability of channels. Results: Western blots demonstrated presence of both AT1 and AT2 AngII receptors in DPDE and CFPAC cells; the density of AT1 receptors appeared lower than that of AT2 receptors. Basal intracellular calcium concentrations did not differ between DPDE (109 ± 11 nM) and CFPAC (103 ± 8 nM) cells. AngII significantly increased measured intracellular calcium concentrations in both DPDE (909 ± 98 nM) and CFPAC (879 ± 207 nM) cells, as did ATP (DPDE = 1722 ± 228 nM; CFPAC = 1522 ± 245 nM). In the patch clamp studies, a variety of different channels were observed; they appeared to be an 11pS nonselective cation (NSC) channel, a 4.6pS Na+ channel, a 3pS anion channel, and an 8pS chloride channel. The latter channel had characteristics similar to cystic fibrosis transmembrane conductance regulator (CFTR). Apical or basolateral application of AngII activated both the 11pS NSC and the 3pS channels. Conclusion: In nontransformed DPDE and CFPAC cells, specific AngII receptors mediate increases in [Ca+2]i. The latter effect of AngII may elicit activation of calcium-mediated chloride channels, suggesting a role for AngII as an alternative mediator of pancreatic ductal secretion.
Persistent Identifierhttp://hdl.handle.net/10722/92520
ISSN
2015 Impact Factor: 2.738
2015 SCImago Journal Rankings: 1.114
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFink, ASen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorMendez, Ten_HK
dc.contributor.authorWorrell, RTen_HK
dc.contributor.authorEaton, Den_HK
dc.contributor.authorNguyen, TDen_HK
dc.contributor.authorLee, SPen_HK
dc.date.accessioned2010-09-17T10:48:44Z-
dc.date.available2010-09-17T10:48:44Z-
dc.date.issued2002en_HK
dc.identifier.citationPancreas, 2002, v. 25 n. 3, p. 290-295en_HK
dc.identifier.issn0885-3177en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92520-
dc.description.abstractIntroduction: Calcium-activated chloride conductance has been identified in normal pancreatic duct cells. Recent in vitro evidence suggests that angiotensin II (AngII) stimulates pancreatic secretion in both cystic fibrosis (CFPAC) and transformed pancreatic cells. Aims: To investigate calcium-mediated stimulatory effects of AngII in both nontransformed dog pancreatic duct epithelial (DPDE) and CFPAC cells. Methods: Western blots were performed in both cells seeking AngII receptors. In additional studies, DPDE and CFPAC cells were grown on vitrogen-coated glass cover slips and loaded with Indo-1-AM dye. Cells were placed in a confocal microscope's perfusion chamber and perfused with 100 μM AngII or ATP (control). Cells were excited with UV light, and intracellular calcium ([Ca+2]i) was read using fluorescence emission at 405 and 530 nm. Finally, single channels in the DPDE cells were examined using cell-attached patch clamps. Current amplitude histograms provided estimates of the conductance and open probability of channels. Results: Western blots demonstrated presence of both AT1 and AT2 AngII receptors in DPDE and CFPAC cells; the density of AT1 receptors appeared lower than that of AT2 receptors. Basal intracellular calcium concentrations did not differ between DPDE (109 ± 11 nM) and CFPAC (103 ± 8 nM) cells. AngII significantly increased measured intracellular calcium concentrations in both DPDE (909 ± 98 nM) and CFPAC (879 ± 207 nM) cells, as did ATP (DPDE = 1722 ± 228 nM; CFPAC = 1522 ± 245 nM). In the patch clamp studies, a variety of different channels were observed; they appeared to be an 11pS nonselective cation (NSC) channel, a 4.6pS Na+ channel, a 3pS anion channel, and an 8pS chloride channel. The latter channel had characteristics similar to cystic fibrosis transmembrane conductance regulator (CFTR). Apical or basolateral application of AngII activated both the 11pS NSC and the 3pS channels. Conclusion: In nontransformed DPDE and CFPAC cells, specific AngII receptors mediate increases in [Ca+2]i. The latter effect of AngII may elicit activation of calcium-mediated chloride channels, suggesting a role for AngII as an alternative mediator of pancreatic ductal secretion.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.pancreasjournal.comen_HK
dc.relation.ispartofPancreasen_HK
dc.subjectAngiotensin IIen_HK
dc.subjectCalcium-mediated chloride channelsen_HK
dc.subjectPancreatic ductal secretionen_HK
dc.titleAngiotensin II evokes calcium-mediated signaling events in isolated dog pancreatic epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailLee, SP: sumlee@hku.hken_HK
dc.identifier.authorityLee, SP=rp01351en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/00006676-200210000-00012en_HK
dc.identifier.pmid12370541-
dc.identifier.scopuseid_2-s2.0-0036786111en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036786111&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue3en_HK
dc.identifier.spage290en_HK
dc.identifier.epage295en_HK
dc.identifier.isiWOS:000178259400012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridFink, AS=7202322385en_HK
dc.identifier.scopusauthoridWang, Y=7601496260en_HK
dc.identifier.scopusauthoridMendez, T=6601983746en_HK
dc.identifier.scopusauthoridWorrell, RT=7006385694en_HK
dc.identifier.scopusauthoridEaton, D=7201566373en_HK
dc.identifier.scopusauthoridNguyen, TD=35546959700en_HK
dc.identifier.scopusauthoridLee, SP=7601417497en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats