File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Up-regulation of the non-neurogenic cholinergic system in the aorta of spontaneously hypertensive rats

TitleUp-regulation of the non-neurogenic cholinergic system in the aorta of spontaneously hypertensive rats
Authors
Issue Date2008
PublisherFederation of American Societies for Experimental Biology. Meeting abstracts can be accessed via http://www.fasebj.org/search.dtl
Citation
Experimental Biology 2008 - ASPET's Centennial Meeting, San Diego, CA, 5-9 April 2008. In The FASEB Journal, 2008, v. 22 n. Meeting Abstract Supplement, p. 912.12 How to Cite?
AbstractDespite the intense interest in the effect of acetylcholine in the vascular system, no evidence has been provided suggesting that endothelial cells are directly innervated by cholinergic neurons. The present study was designed to test whether or not the rat aorta contain the biochemical apparatus needed to synthesize, transport, store and degrade acetylcholine, and if so, whether or not differences in the expression of these components exist between preparations from normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Gene expressions were quantified by real-time PCR. The mRNA expression for the neuronal choline acetyltransferase (which synthesizes acetylcholine from the substrates acetyl CoA and choline), vesicular acetylcholine transporter (which specializes in the trafficking of acetylcholine) and acetylcholine esterase (which breakdowns acetylcholine) were expressed in the aorta of both WKY and SHR. The expression of these enzymes was significantly higher in the latter. These data suggest that acetylcholine synthesis is not limited to the cholinergic nerves, but that the cholinergic transmitter is released directly from the aorta in an autocrine fashion to modulate local blood flow. The enhanced vascular synthesis of acetylcholine in the hypertensive rat may reflect a compensatory response to correct for endothelial dysfunction. This work is funded by the RGC – HKU.
Persistent Identifierhttp://hdl.handle.net/10722/106844
ISSN
2021 Impact Factor: 5.834
2020 SCImago Journal Rankings: 1.709

 

DC FieldValueLanguage
dc.contributor.authorTang, EHCen_HK
dc.contributor.authorVanhoutte, PMGRen_HK
dc.date.accessioned2010-09-25T23:32:46Z-
dc.date.available2010-09-25T23:32:46Z-
dc.date.issued2008en_HK
dc.identifier.citationExperimental Biology 2008 - ASPET's Centennial Meeting, San Diego, CA, 5-9 April 2008. In The FASEB Journal, 2008, v. 22 n. Meeting Abstract Supplement, p. 912.12en_HK
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/106844-
dc.description.abstractDespite the intense interest in the effect of acetylcholine in the vascular system, no evidence has been provided suggesting that endothelial cells are directly innervated by cholinergic neurons. The present study was designed to test whether or not the rat aorta contain the biochemical apparatus needed to synthesize, transport, store and degrade acetylcholine, and if so, whether or not differences in the expression of these components exist between preparations from normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Gene expressions were quantified by real-time PCR. The mRNA expression for the neuronal choline acetyltransferase (which synthesizes acetylcholine from the substrates acetyl CoA and choline), vesicular acetylcholine transporter (which specializes in the trafficking of acetylcholine) and acetylcholine esterase (which breakdowns acetylcholine) were expressed in the aorta of both WKY and SHR. The expression of these enzymes was significantly higher in the latter. These data suggest that acetylcholine synthesis is not limited to the cholinergic nerves, but that the cholinergic transmitter is released directly from the aorta in an autocrine fashion to modulate local blood flow. The enhanced vascular synthesis of acetylcholine in the hypertensive rat may reflect a compensatory response to correct for endothelial dysfunction. This work is funded by the RGC – HKU.-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. Meeting abstracts can be accessed via http://www.fasebj.org/search.dtl-
dc.relation.ispartofThe FASEB Journalen_HK
dc.titleUp-regulation of the non-neurogenic cholinergic system in the aorta of spontaneously hypertensive ratsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hken_HK
dc.identifier.hkuros152584en_HK
dc.identifier.spage171en_HK
dc.identifier.issnl0892-6638-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats