File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: An indispensable role of secretin in mediating the osmoregulatory functions of angiotensin II

TitleAn indispensable role of secretin in mediating the osmoregulatory functions of angiotensin II
Authors
Issue Date2010
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Faseb Journal, 2010, v. 24 n. 12, p. 5024-5032 How to Cite?
AbstractFluid balance is critical to life and hence is tightly controlled in the body. Angiotensin II (ANGII), one of the most important components of this regulatory system, is recognized as a dipsogenic hormone that stimulates vasopressin (VP) expression and release. However, detailed mechanisms regarding how ANGII brings about these changes are not fully understood. In the present study, we show initially that the osmoregulatory functions of secretin (SCT) in the brain are similar to those of ANGII in mice and, more important, we discovered the role of SCT as the link between ANGII and its downstream effects. This was substantiated by the use of two knockout mice, SCTR -/- and SCT -/-, in which we show the absence of an intact SCT/secretin receptor (SCTR) axis resulted in an abolishment or much reduced ANGII osmoregulatory functions. By immunohistochemical staining and in situ hybridization, the proteins and transcripts of SCT and its receptor are found in the paraventricular nucleus (PVN) and lamina terminalis. We propose that SCT produced in the circumventricular organs is transported and released in the PVN to stimulate vasopressin expression and release. In summary, our findings identify SCT and SCTR as novel elements of the ANGII osmoregulatory pathway in maintaining fluid balance in the body. © FASEB.
Persistent Identifierhttp://hdl.handle.net/10722/179215
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, VHYen_US
dc.contributor.authorLee, LTOen_US
dc.contributor.authorChu, JYSen_US
dc.contributor.authorLam, IPYen_US
dc.contributor.authorSiu, FKYen_US
dc.contributor.authorVaudry, Hen_US
dc.contributor.authorChow, BKCen_US
dc.date.accessioned2012-12-19T09:53:00Z-
dc.date.available2012-12-19T09:53:00Z-
dc.date.issued2010en_US
dc.identifier.citationFaseb Journal, 2010, v. 24 n. 12, p. 5024-5032en_US
dc.identifier.issn0892-6638en_US
dc.identifier.urihttp://hdl.handle.net/10722/179215-
dc.description.abstractFluid balance is critical to life and hence is tightly controlled in the body. Angiotensin II (ANGII), one of the most important components of this regulatory system, is recognized as a dipsogenic hormone that stimulates vasopressin (VP) expression and release. However, detailed mechanisms regarding how ANGII brings about these changes are not fully understood. In the present study, we show initially that the osmoregulatory functions of secretin (SCT) in the brain are similar to those of ANGII in mice and, more important, we discovered the role of SCT as the link between ANGII and its downstream effects. This was substantiated by the use of two knockout mice, SCTR -/- and SCT -/-, in which we show the absence of an intact SCT/secretin receptor (SCTR) axis resulted in an abolishment or much reduced ANGII osmoregulatory functions. By immunohistochemical staining and in situ hybridization, the proteins and transcripts of SCT and its receptor are found in the paraventricular nucleus (PVN) and lamina terminalis. We propose that SCT produced in the circumventricular organs is transported and released in the PVN to stimulate vasopressin expression and release. In summary, our findings identify SCT and SCTR as novel elements of the ANGII osmoregulatory pathway in maintaining fluid balance in the body. © FASEB.en_US
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_US
dc.relation.ispartofFASEB Journalen_US
dc.subject.meshAngiotensin Ii - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDrinking - Drug Effectsen_US
dc.subject.meshFemaleen_US
dc.subject.meshHypothalamus - Drug Effects - Metabolismen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshIn Situ Hybridizationen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshParaventricular Hypothalamic Nucleus - Drug Effects - Metabolismen_US
dc.subject.meshPituitary Gland - Drug Effects - Metabolismen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshReceptors, G-Protein-Coupled - Genetics - Metabolismen_US
dc.subject.meshReceptors, Gastrointestinal Hormone - Genetics - Metabolismen_US
dc.subject.meshSecretin - Genetics - Metabolism - Pharmacologyen_US
dc.subject.meshVasopressins - Metabolismen_US
dc.subject.meshWater-Electrolyte Balance - Drug Effectsen_US
dc.titleAn indispensable role of secretin in mediating the osmoregulatory functions of angiotensin IIen_US
dc.typeArticleen_US
dc.identifier.emailLee, LTO: ltolee2@hkucc.hku.hken_US
dc.identifier.emailChu, JYS: hitan@graduate.hku.hken_US
dc.identifier.emailChow, BKC: bkcc@hku.hken_US
dc.identifier.authorityLee, LTO=rp00727en_US
dc.identifier.authorityChu, JYS=rp00684en_US
dc.identifier.authorityChow, BKC=rp00681en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1096/fj.10-165399en_US
dc.identifier.pmid20739612-
dc.identifier.scopuseid_2-s2.0-78649747023en_US
dc.identifier.hkuros185541-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78649747023&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume24en_US
dc.identifier.issue12en_US
dc.identifier.spage5024en_US
dc.identifier.epage5032en_US
dc.identifier.eissn1530-6860-
dc.identifier.isiWOS:000284824400040-
dc.publisher.placeUnited Statesen_US
dc.identifier.f100010505956-
dc.identifier.scopusauthoridLee, VHY=14050662700en_US
dc.identifier.scopusauthoridLee, LTO=8367269000en_US
dc.identifier.scopusauthoridChu, JYS=34975209300en_US
dc.identifier.scopusauthoridLam, IPY=14050702700en_US
dc.identifier.scopusauthoridSiu, FKY=6701518484en_US
dc.identifier.scopusauthoridVaudry, H=35446602600en_US
dc.identifier.scopusauthoridChow, BKC=7102826193en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats