File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)

Conference Paper: Secretin: a neurosecretory factor regulating body water homeostasis

TitleSecretin: a neurosecretory factor regulating body water homeostasis
Authors
KeywordsMedical sciences
Psychiatry and neurology
Issue Date2010
PublisherHumana Press, Inc.
Citation
The 9th International Symposium on VIP, PACAP and Related Peptides, Kagoshima, Japan, 5-8 October 2009. In Journal of Molecular Neuroscience, 2010, v. 42 n. 3, p. 285 How to Cite?
AbstractVasopressin (Vp) and oxytocin (Oxt) are generally accepted to be the only two neurosecretory hormones that are released from the posterior pituitary into the systemic circulation. However, recent findings from our group showed that secretin, originally isolated from the upper intestinal mucosal extract, is abundantly expressed in the hypothalamic magnocellular neurons and is also a neuro-secretory hormone that is released from the posterior pituitary into the systemic circulation under plasma hyperosmolality conditions. Using secretin-null (SCT-/-) and secretin receptor-null (SCTR-/-) mice, we found that mutation of either genes could alter the expression and release of Vp under plasma hyperosmolality. Additionally, reduction in the renal expression of water channels including aquaporin-2 and aquaporin-4, as well as altered glomerular and tubular morphology, were also observed in these transgenic littermates. Together with the findings that secretin could (1) act as a dipsogenic agent when injected intracerebroventricularly and (2) directly stimulate the expression and translocation of the aquaporin-2 in the renal medullary tubules, we propose here that the peptide could work at multiple levels in the subfornical organ-hypothalamopituitary-kidney axis to regulate body water homeostasis. These findings not only challenge our previous understanding regarding the neuroanatomy of neurohypophysis, but also provide information for at least one of the Vp-independent mechanisms that modulate the process of renal water reabsorption. Future investigations in this direction should be important in developing therapeutic means for treating Xlinked nephrogenic diabetes insipidus by therapeutically bypassing the dysfunctional Vp receptors.
DescriptionSession 5: Endocrine System and Metabolism: no. PL5
This journal issue entitled: Special Issue: VIP, PACAP and Related Peptides
Persistent Identifierhttp://hdl.handle.net/10722/127815
ISSN
2015 Impact Factor: 2.352
2015 SCImago Journal Rankings: 0.988

 

DC FieldValueLanguage
dc.contributor.authorChu, JYSen_HK
dc.contributor.authorLee, LTOen_HK
dc.contributor.authorChan, YSen_HK
dc.contributor.authorChow, BKCen_HK
dc.date.accessioned2010-10-31T13:48:08Z-
dc.date.available2010-10-31T13:48:08Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 9th International Symposium on VIP, PACAP and Related Peptides, Kagoshima, Japan, 5-8 October 2009. In Journal of Molecular Neuroscience, 2010, v. 42 n. 3, p. 285en_HK
dc.identifier.issn0895-8696-
dc.identifier.urihttp://hdl.handle.net/10722/127815-
dc.descriptionSession 5: Endocrine System and Metabolism: no. PL5-
dc.descriptionThis journal issue entitled: Special Issue: VIP, PACAP and Related Peptides-
dc.description.abstractVasopressin (Vp) and oxytocin (Oxt) are generally accepted to be the only two neurosecretory hormones that are released from the posterior pituitary into the systemic circulation. However, recent findings from our group showed that secretin, originally isolated from the upper intestinal mucosal extract, is abundantly expressed in the hypothalamic magnocellular neurons and is also a neuro-secretory hormone that is released from the posterior pituitary into the systemic circulation under plasma hyperosmolality conditions. Using secretin-null (SCT-/-) and secretin receptor-null (SCTR-/-) mice, we found that mutation of either genes could alter the expression and release of Vp under plasma hyperosmolality. Additionally, reduction in the renal expression of water channels including aquaporin-2 and aquaporin-4, as well as altered glomerular and tubular morphology, were also observed in these transgenic littermates. Together with the findings that secretin could (1) act as a dipsogenic agent when injected intracerebroventricularly and (2) directly stimulate the expression and translocation of the aquaporin-2 in the renal medullary tubules, we propose here that the peptide could work at multiple levels in the subfornical organ-hypothalamopituitary-kidney axis to regulate body water homeostasis. These findings not only challenge our previous understanding regarding the neuroanatomy of neurohypophysis, but also provide information for at least one of the Vp-independent mechanisms that modulate the process of renal water reabsorption. Future investigations in this direction should be important in developing therapeutic means for treating Xlinked nephrogenic diabetes insipidus by therapeutically bypassing the dysfunctional Vp receptors.-
dc.languageengen_HK
dc.publisherHumana Press, Inc.-
dc.relation.ispartofJournal of Molecular Neuroscience-
dc.rightsThe original publication is available at www.springerlink.com-
dc.subjectMedical sciences-
dc.subjectPsychiatry and neurology-
dc.titleSecretin: a neurosecretory factor regulating body water homeostasisen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0895-8696&volume=42&issue=3&spage=285&epage=&date=2009&atitle=Secretin:+a+neurosecretory+factor+regulating+body+water+homeostasis-
dc.identifier.emailChu, JYS: hitan@graduate.hku.hken_HK
dc.identifier.emailLee, LTO: ltolee2@hkucc.hku.hken_HK
dc.identifier.emailChan, YS: yschan@hkucc.hku.hken_HK
dc.identifier.emailChow, BKC: bkcc@hkusua.hku.hken_HK
dc.identifier.doi10.1007/s12031-009-9324-2-
dc.identifier.hkuros176313en_HK
dc.identifier.volume42-
dc.identifier.issue3-
dc.identifier.spage285-
dc.identifier.epage285-
dc.description.otherThe 9th International Symposium on VIP, PACAP and Related Peptides, Kagoshima, Japan, 5-8 October 2009. In Journal of Molecular Neuroscience, 2010, v. 42 n. 3, p. 285-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats