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Article: Increased endogenous nitric oxide release by iron chelation and purinergic activation in the rat carotid body

TitleIncreased endogenous nitric oxide release by iron chelation and purinergic activation in the rat carotid body
Authors
KeywordsCarotid chemoreceptor
HIF
Hypoxia
NO synthase
Purinergic receptor
Issue Date2007
PublisherBentham Open. The Journal's web site is located at http://www.bentham.org/open/tobiocj/
Citation
The Open Biochemistry Journal, 2007, v. 1, p. 1-6 How to Cite?
AbstractWe examined the hypothesis that hypoxic chemotransduction with stabilization of HIF-1 and activation of purinoceptors stimulate the endogenous NO production in the rat carotid body. The effects of blockade of purinoceptors with suramin, or blockade of HIF-1alpha hydroxylation by suppressing prolyl hydroxylase (PAH) activity on the endogenous NO release measured electrochemically by microsensor inserted into the isolated carotid body superfused with bicarbonate-buffer were examined. Suramin did not change the resting NO level under normoxic conditions but it significantly decreased the hypoxia-induced NO elevation in a dose-dependent manner. Suramin (100muM) blocked the NO response to acute hypoxia by 53%. Intracellular iron chelator, ciclopirox olamine (CPX) significantly increased the resting NO release close to the hypoxic level, which was reversed by FeSO(4) or blocked by L-NMMA. Also, PAH inhibition with dimethy-loxalylglycine (DMOG) moderately increased the resting NO release. In the presence of CPX and DMOG the resting NO release was increased to the hypoxic level. Collectively, results suggest that iron chelation and purinoceptor stimulation play a role in the hypoxic chemotransduction for an increase in the endogenous NO production in the rat carotid body.
Persistent Identifierhttp://hdl.handle.net/10722/81365
ISSN
2015 SCImago Journal Rankings: 0.445
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorFung, MLen_HK
dc.contributor.authorLi, Men_HK
dc.contributor.authorLahiri, Sen_HK
dc.date.accessioned2010-09-06T08:16:48Z-
dc.date.available2010-09-06T08:16:48Z-
dc.date.issued2007en_HK
dc.identifier.citationThe Open Biochemistry Journal, 2007, v. 1, p. 1-6en_HK
dc.identifier.issn1874-091X-
dc.identifier.urihttp://hdl.handle.net/10722/81365-
dc.description.abstractWe examined the hypothesis that hypoxic chemotransduction with stabilization of HIF-1 and activation of purinoceptors stimulate the endogenous NO production in the rat carotid body. The effects of blockade of purinoceptors with suramin, or blockade of HIF-1alpha hydroxylation by suppressing prolyl hydroxylase (PAH) activity on the endogenous NO release measured electrochemically by microsensor inserted into the isolated carotid body superfused with bicarbonate-buffer were examined. Suramin did not change the resting NO level under normoxic conditions but it significantly decreased the hypoxia-induced NO elevation in a dose-dependent manner. Suramin (100muM) blocked the NO response to acute hypoxia by 53%. Intracellular iron chelator, ciclopirox olamine (CPX) significantly increased the resting NO release close to the hypoxic level, which was reversed by FeSO(4) or blocked by L-NMMA. Also, PAH inhibition with dimethy-loxalylglycine (DMOG) moderately increased the resting NO release. In the presence of CPX and DMOG the resting NO release was increased to the hypoxic level. Collectively, results suggest that iron chelation and purinoceptor stimulation play a role in the hypoxic chemotransduction for an increase in the endogenous NO production in the rat carotid body.-
dc.languageengen_HK
dc.publisherBentham Open. The Journal's web site is located at http://www.bentham.org/open/tobiocj/-
dc.relation.ispartofThe Open Biochemistry Journalen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCarotid chemoreceptor-
dc.subjectHIF-
dc.subjectHypoxia-
dc.subjectNO synthase-
dc.subjectPurinergic receptor-
dc.titleIncreased endogenous nitric oxide release by iron chelation and purinergic activation in the rat carotid bodyen_HK
dc.typeArticleen_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.2174/1874091X00701010001-
dc.identifier.pmid18949066-
dc.identifier.pmcidPMC2570544-
dc.identifier.hkuros128804en_HK
dc.identifier.volume1-
dc.identifier.spage1-
dc.identifier.epage6-
dc.publisher.placeNetherlands-

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