Salt and Nitric Oxide Inhibition Induced Hypertension: The Role of Prostacycline and 8-Isoprostane

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dc.authoridOktar, Suleyman/0000-0003-0151-5981
dc.contributor.authorIlhan, Selcuk
dc.contributor.authorOktar, Suleyman
dc.contributor.authorSahna, Engin
dc.contributor.authorAksulu, Hakki Engin
dc.date.accessioned2025-01-27T20:45:41Z
dc.date.available2025-01-27T20:45:41Z
dc.date.issued2011
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
dc.description.abstractRenal prostacycline (PGI(2)) and oxidative stress are known to be important factors that effect the natriurezis and diuresis. 8-iso prostaglandin F-2 alpha (8-isoprostane), a member of F-2-isoprostanes, is formed from the nonenzymatic reaction of arachidonic acid and oxygen radicals in vivo and in vitro, and also it is a marker of oxidative stress in vivo. The aim of this study is to determine the role of renal PGI(2) and 8-isoprostane in a salt and nitric oxide (NO) inhibition-induced hypertension model. Rats were distributed equally among four groups (n = 6 per group). Control rats were given normal salt diet (0.32%); high-salt (HS) rats were given high salt diet (3.2%); NG-nitro-L-arginine (L-NNA) rats were given normal salt diet and 25 mg/kg L-NNA; HS+L-NNA rats were given high salt diet and 25 mg/kg L-NNA. Rats were placed in individual metabolic cages for 17 days. Systolic blood pressure (SBP) was measured at days initial, 7th and 14th. Urinary 8-isoprostane and PGI(2) levels were analyzed. Salt-loading alone did not change SBP values. The average SBP in L-NNA and HS+L-NNA groups were shown to significantly enhance compared to initial and day 7th in the same groups, respectively. The levels of 8-isoprostane in the HS+L-NNA group was significantly enhanced compared to the other groups. L-NNA or HS diet alone did not change the levels of 8-isoprostane compared to the control group. L-NNA alone did not change PGI(2) levels in urine compared to the control. PGI(2) levels in the HS, and the HS+L-NNA group was significantly higher compared to the control group. This study concluded that NOS inhibition plus salt-loading induced oxidative stress and increased renal PGI(2). Also, it is suggested that augmented oxidative stress may aggravate the hypertension. But the renal synthesis of PGI(2) is increased in order to augment the diuresis and natriuresis without the effect of blood pressure (BP).
dc.identifier.doi10.3109/10641963.2010.503305
dc.identifier.endpage88
dc.identifier.issn1064-1963
dc.identifier.issn1525-6006
dc.identifier.issue2
dc.identifier.pmid21214402
dc.identifier.scopus2-s2.0-79952922789
dc.identifier.scopusqualityQ2
dc.identifier.startpage84
dc.identifier.urihttps://doi.org/10.3109/10641963.2010.503305
dc.identifier.urihttps://hdl.handle.net/20.500.12428/24682
dc.identifier.volume33
dc.identifier.wosWOS:000288550000003
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis Inc
dc.relation.ispartofClinical and Experimental Hypertension
dc.relation.publicationcategoryinfo:eu-repo/semantics/openAccess
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20250125
dc.subjectnitric oxide (NO)
dc.subject8-isoprostane
dc.subjectprostacyclin
dc.subjectsalt-loading
dc.subjecthypertension
dc.titleSalt and Nitric Oxide Inhibition Induced Hypertension: The Role of Prostacycline and 8-Isoprostane
dc.typeArticle

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