Nitric oxide and oxidative stress in atherosclerotic renovascular hypertension: Effect of endovascular treatment

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dc.contributor.authorParildar, M
dc.contributor.authorParildar, Z
dc.contributor.authorOran, I
dc.contributor.authorKabaroglu, C
dc.contributor.authorMemis, A
dc.contributor.authorBayindir, O
dc.date.accessioned2019-10-27T18:39:12Z
dc.date.available2019-10-27T18:39:12Z
dc.date.issued2003
dc.departmentEge Üniversitesien_US
dc.description.abstractPURPOSE: Because activation of the renin-angiotensin system leads to an increase in oxidative stress, the authors investigated nitric oxide (NO; nitrite + nitrate), superoxide dismutase (SOD), catalase, and malondialdehyde (MDA) levels and the effect of endovascular treatment on these parameters in patients with atherosclerotic renovascular hypertension. The relationship of NO with blood pressure and renal functional indexes was also investigated. MATERIALS AND METHODS: In this prospective cohort study, serum creatinine, NO, SOD, catalase, plasma MDA, urinary microalbumin, and NO levels, and blood pressure were determined in 21 patients with hypertension and unilateral renal artery stenosis caused by atherosclerosis at entry and after 24 hours, 2 weeks, and 6 weeks of endovascular treatment. RESULTS: MDA concentrations decreased 24 hours after intervention and remained low 2 and 6 weeks later. In addition, serum SOD and NO and urine NO levels were increased significantly 24 hours after endovascular treatment and decreased after 2 and 6 weeks. However, serum catalase levels did not differ after the intervention. Blood pressures decreased after treatment. There were no significant differences in urinary microalbumin levels, estimated glomerular filtration rates, and creatinine levels after endovascular treatment. CONCLUSIONS: Endovascular treatment decreases oxidative stress and may offer new benefits in the treatment of patients with hypertension associated with renal artery stenosis. The decrease in oxidative stress and/or the upregulation of SOD may increase the bioavailability of NO, which in turn may lead to the rapid hypotensive response.en_US
dc.identifier.doi10.1097/01.RVI.0000083841.97061.12en_US
dc.identifier.endpage892en_US
dc.identifier.issn1051-0443
dc.identifier.issue7en_US
dc.identifier.pmid12847196en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage887en_US
dc.identifier.urihttps://doi.org/10.1097/01.RVI.0000083841.97061.12
dc.identifier.urihttps://hdl.handle.net/11454/36732
dc.identifier.volume14en_US
dc.identifier.wosWOS:000184102500008en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherLippincott Williams & Wilkinsen_US
dc.relation.ispartofJournal of Vascular and Interventional Radiologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.titleNitric oxide and oxidative stress in atherosclerotic renovascular hypertension: Effect of endovascular treatmenten_US
dc.typeArticleen_US

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