Effect of glycerol on endothelium-derived factors in the vasculature of the rabbit kidney

dc.contributor.authorSipahi, Emine Y.
dc.contributor.authorKeskil, Zuhal A.
dc.contributor.authorErdinç, Meral
dc.contributor.authorNergis, Yusuf
dc.contributor.authorTürker, R. Kazım
dc.contributor.authorErcan, Z. Sevim
dc.date.accessioned2020-06-25T15:13:15Z
dc.date.available2020-06-25T15:13:15Z
dc.date.issued2002
dc.departmentKırıkkale Üniversitesi
dc.description.abstract1. In the present study, endothelium-derived relaxing factor (EDRF/nitric oxide (NO)), conversion of big endothelin (ET)-1 to endothelin-1 (ET-1) and the role of reactive oxygen species were investigated in kidneys isolated from glycerol (GLY)-pretreated rabbits. 2. Acetylcholine (ACh)-induced vasodilation that is due to the release of EDRF/NO is significantly decreased, whereas big ET-1-induced vasoconstriction was increased in kidneys isolated from GLY-pretreated rabbits. 3. Pretreatment of rabbits with the xanthine oxidase inhibitor allopurinol and the NO precursor L-arginine reversed the inhibition of ACh-induced vasodilation due to GLY and protects the kidney vasculature. 4. Big ET-1, but not ET-1, responses were found to be significantly increased in kidneys isolated from GLY-pretreated rabbits. This increase is attributed to the higher conversion rate of big ET-1 to ET-1 because the ET-converting enzyme (ECE) inhibitor phosphoramidon, at a concentration of 10-6 mol/L, causes an inhibition in the response to big ET-1 by 52.6% in normal kidneys, whereas this inhibition with the same concentration of phosphoramidon was found to be significantly decreased in kidneys isolated from GLY-pretreated rabbits. 5. The non-selective NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) caused a significant potentiation in the vasoconstrictor response to ET-1 in normal isolated perfused rabbit kidneys. However, L-NAME did not alter the responses to ET-1 in GLY-pretreated kidneys. 6. These results indicate that accumulation of reactive oxygen species causes an inhibition in NO bioavailability. Increased conversion of big ET-1 to ET-1 may also contribute to the mechanism of vascular damage due to GLY.en_US
dc.identifier.citationclosedAccessen_US
dc.identifier.doi10.1046/j.1440-1681.2002.03716.x
dc.identifier.endpage683en_US
dc.identifier.issn03051870
dc.identifier.issue8en_US
dc.identifier.pmid12099999
dc.identifier.scopus2-s2.0-0035988903
dc.identifier.scopusqualityQ2
dc.identifier.startpage679en_US
dc.identifier.urihttps://doi.org/10.1046/j.1440-1681.2002.03716.x
dc.identifier.urihttps://hdl.handle.net/20.500.12587/1690
dc.identifier.volume29en_US
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.relation.ispartofClinical and Experimental Pharmacology and Physiology
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectEndothelin-converting enzymeen_US
dc.subjectEndothelium-derived relaxing factor/nitric oxideen_US
dc.subjectGlycerolen_US
dc.subjectL-arginineen_US
dc.subjectRabbit kidneyen_US
dc.subjectReactive oxygen speciesen_US
dc.titleEffect of glycerol on endothelium-derived factors in the vasculature of the rabbit kidneyen_US
dc.typeArticle

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