An analysis of the impact of buthionine sulfoximine and N-nitro-L-arginine on blood pressure

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dc.contributor.authorGungor, Buket
dc.contributor.authorAkdur, Secil
dc.contributor.authorSılan, Coşkun
dc.contributor.authorCoskun, Ozlem
dc.contributor.authorAksulu, Hakki Engin
dc.date.accessioned2025-01-27T20:43:39Z
dc.date.available2025-01-27T20:43:39Z
dc.date.issued2023
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
dc.description.abstractIntroduction: The presence of weaknesses in the efficacy of endogenous natriuretic and vasodilator agents plays a significant role in developing high blood pressure. It is often suggested that oxidative stress is critical in developing hypertension due to nitric oxide synthase (NOS) inhibition. This study aimed to investigate the intrarenal dopaminergic system activities, involvement of oxidative stress, and blood pressure changes resulting from NOS inhibition with N-nitro-L-arginine (L-NNA) and/or L-buthionine sulfoximine (BSO).Methods: Male Wistar albino rats (n = 24) were administered water containing 50 mg/L L-NNA for 21 days and/or intraperitoneal injections of BSO (125 mg/kg twice daily) for seven days; control rats were administered tap water. The rats' blood pressure; water and salt balance; total oxidant and antioxidant capacities; and urinary dopamine, adrenaline, and noradrenaline levels were measured.Results: While L-NNA and BSO alone did not significantly alter blood pressure, their coadministration caused rats to develop hypertension and significantly reduced the fractional excretion of sodium, increasing its tubular reabsorption. Urinary dopamine levels, indicators of intrarenal dopamine synthesis, did not change significantly Conclusion: These results indicate the importance of the weakness of endogenous natriuretic systems such as nitric oxide in hypertension development. While BSO did not induce oxidative stress in the measured parameters, it was shown for the first time as an actor in hypertension development in subjects with NOS inhibition to the extent that such inhibition did not increase blood pressure.
dc.description.sponsorshipOffice of Scientific Research Projects at Canakkale Onsekiz Mart University [2010/83]
dc.description.sponsorshipThis study was supported by the Office of Scientific Research Projects at Canakkale Onsekiz Mart University (project number: 2010/83) .
dc.identifier.doi10.15419/bmrat.v10i6.814
dc.identifier.endpage5743
dc.identifier.issn2198-4093
dc.identifier.issue6
dc.identifier.scopus2-s2.0-85192652165
dc.identifier.scopusqualityN/A
dc.identifier.startpage5735
dc.identifier.urihttps://doi.org/10.15419/bmrat.v10i6.814
dc.identifier.urihttps://hdl.handle.net/20.500.12428/24313
dc.identifier.volume10
dc.identifier.wosWOS:001059459800002
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherBiomedpress
dc.relation.ispartofBiomedical Research and Therapy
dc.relation.publicationcategoryinfo:eu-repo/semantics/openAccess
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20250125
dc.subjectBSO
dc.subjectHypertension
dc.subjectL-NNA
dc.subjectOxidative stress
dc.subjectTRFNa
dc.titleAn analysis of the impact of buthionine sulfoximine and N-nitro-L-arginine on blood pressure
dc.typeArticle

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