Effect of glycerol on endothelium-derived factors in the vasculature of the rabbit kidney
dc.contributor.author | Sipahi, EY | |
dc.contributor.author | Keskil, ZA | |
dc.contributor.author | Erdinç, M | |
dc.contributor.author | Nergis, Y | |
dc.contributor.author | Türker, RK | |
dc.contributor.author | Ercan, ZS | |
dc.date.accessioned | 2024-04-24T16:24:06Z | |
dc.date.available | 2024-04-24T16:24:06Z | |
dc.date.issued | 2002 | |
dc.department | Dicle Üniversitesi | en_US |
dc.description.abstract | 1. 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 N (G) -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.doi | 10.1046/j.1440-1681.2002.03716.x | |
dc.identifier.endpage | 683 | en_US |
dc.identifier.issn | 0305-1870 | |
dc.identifier.issn | 1440-1681 | |
dc.identifier.issue | 8 | en_US |
dc.identifier.pmid | 12099999 | |
dc.identifier.scopus | 2-s2.0-0035988903 | |
dc.identifier.scopusquality | Q2 | |
dc.identifier.startpage | 679 | en_US |
dc.identifier.uri | https://doi.org/10.1046/j.1440-1681.2002.03716.x | |
dc.identifier.uri | https://hdl.handle.net/11468/16486 | |
dc.identifier.volume | 29 | en_US |
dc.identifier.wos | WOS:000176639600007 | |
dc.identifier.wosquality | Q3 | |
dc.indekslendigikaynak | Web of Science | |
dc.indekslendigikaynak | Scopus | |
dc.indekslendigikaynak | PubMed | |
dc.language.iso | en | en_US |
dc.publisher | Wiley | en_US |
dc.relation.ispartof | Clinical and Experimental Pharmacology and Physiology | |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | L-Arginine | en_US |
dc.subject | Endothelin-Converting Enzyme | en_US |
dc.subject | Endothelium-Derived Relaxing Factor | en_US |
dc.subject | Nitric Oxide | en_US |
dc.subject | Glycerol | en_US |
dc.subject | Rabbit Kidney | en_US |
dc.subject | Reactive Oxygen Species | en_US |
dc.title | Effect of glycerol on endothelium-derived factors in the vasculature of the rabbit kidney | en_US |
dc.title | Effect of glycerol on endothelium-derived factors in the vasculature of the rabbit kidney | |
dc.type | Article | en_US |