Salt and Nitric Oxide Synthase Inhibition-Induced Hypertension: Kidney Dysfunction and Brain Anti-Oxidant Capacity

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dc.authoridMEYDAN, SEDAT/0000-0002-1393-3235
dc.authoridOktar, Suleyman/0000-0003-0151-5981
dc.authoridYonden, Zafer/0000-0003-0708-5417
dc.contributor.authorOktar, Suleyman
dc.contributor.authorIlhan, Selcuk
dc.contributor.authorMeydan, Sedat
dc.contributor.authorAydin, Mehmet
dc.contributor.authorYonden, Zafer
dc.contributor.authorGokce, Ahmet
dc.date.accessioned2024-09-18T20:28:17Z
dc.date.available2024-09-18T20:28:17Z
dc.date.issued2010
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractThe specific aim of this study was to examine the effects of salt-loading on kidney function and brain antioxidant capacity. Wistar rats were divided into four groups: Control rats were given normal drinking water and no drug treatment for 2 weeks. LNNA group: rats were given normal drinking water and the nitric oxide (NO) inhibitor NG-nitro-L-arginine (L-NNA), 3 mg/kg/day. LNNA + Salt group: rats were given drinking water containing salt 2% and 3 mg/kg L-NNA. Salt group: rats were given drinking water containing salt 2% and no drug treatment. Basal blood pressure and the levels of serum BUN, creatinine, uric acid, cortisol, electrolyte, serum antioxidant capacity, and oxidative stress were measured. NO, superoxide dismutase (SOD), and catalase (CAT) levels were measured in the hypothalamus, brainstem, and cerebellum. Salt overload increased the blood pressure of the LNNA + Salt group. Salt-loading enhanced BUN, creatinine, sodium retention. High salt produced an increase in uric acid levels and a decrease in cortisol levels in serum. Additionally, the oxidative stress index in serum increased in the LNNA + Salt group. Salt-loading enhanced brain NO levels, but not SOD and CAT activity. L-NNA increased brain SOD activity, but not CAT and NO levels. In conclusion, salt-loading causes hypertension, kidney dysfunction, and enhances oxidative stress in salt-sensitive rats.en_US
dc.description.sponsorshipMustafa Kemal University [08T1502]en_US
dc.description.sponsorshipThis study was supported by the Research Fund of Mustafa Kemal University (08T1502).en_US
dc.identifier.doi10.3109/10641961003628486
dc.identifier.endpage357en_US
dc.identifier.issn1064-1963
dc.identifier.issn1525-6006
dc.identifier.issue6en_US
dc.identifier.pmid21028998en_US
dc.identifier.scopus2-s2.0-78049418484en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage352en_US
dc.identifier.urihttps://doi.org/10.3109/10641961003628486
dc.identifier.urihttps://hdl.handle.net/20.500.12483/10824
dc.identifier.volume32en_US
dc.identifier.wosWOS:000283593900006en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Incen_US
dc.relation.ispartofClinical and Experimental Hypertensionen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectkidneyen_US
dc.subjecthypertensionen_US
dc.subjectoxidative stressen_US
dc.subjectsuperoxide dismutaseen_US
dc.subjectsalten_US
dc.titleSalt and Nitric Oxide Synthase Inhibition-Induced Hypertension: Kidney Dysfunction and Brain Anti-Oxidant Capacityen_US
dc.typeArticleen_US

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