Effects of <i>N</i>‐nitro <scp>l</scp>‐arginine methyl ester (<scp>l</scp>‐NAME), a potent nitric oxide synthase inhibitor, on visual evoked potentials of rats exposed to different experimental stress models

Yargiçoğlu, Pi̇raye; Yaraş, Nazmi; Ağar, Ayşel; Gümüşlü, Saadet; Abidin, İsmail; Bîlmen, Süreyya

doi:10.1111/j.0001-6772.2003.01254.x

Cited by 10 publications

(5 citation statements)

References 46 publications

(62 reference statements)

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“…The administration of L-NAME is often associated with increased production of secondary products of oxidative stress [ 77 – 80 ]. A short-term (2 weeks) administration of L-NAME reduces the activity of glutathione peroxidase and stimulates lipid peroxidation and the level of TBARS in rat brain [ 81 ]. Chronic administration of L-NAME results in an increase of malondialdehyde (MDA) in the hippocampal region of the brain [ 82 ].…”

Section: Discussionmentioning

confidence: 99%

Age-dependent redox status in the brain stem of NO-deficient hypertensive rats

et al. 2017

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BackgroundThe brain stem contains important nuclei that control cardiovascular function via the sympathetic nervous system (SNS), which is strongly influenced by nitric oxide. Its biological activity is also largely determined by oxygen free radicals. Despite many experimental studies, the role of AT1R-NAD(P)H oxidase-superoxide pathway in NO-deficiency is not yet sufficiently clarified. We determined changes in free radical signaling and antioxidant and detoxification response in the brain stem of young and adult Wistar rats during chronic administration of exogenous NO inhibitors.MethodsYoung (4 weeks) and adult (10 weeks) Wistar rats were treated with 7-nitroindazole (7-NI group, 10 mg/kg/day), a specific nNOS inhibitor, with NG-nitro-L-arginine-methyl ester (L-NAME group, 50 mg/kg/day), a nonspecific NOS inhibitor, and with drinking water (Control group) during 6 weeks. Systolic blood pressure was measured by non-invasive plethysmography. Expression of genes (AT1R, AT2R, p22phox, SOD and NOS isoforms, HO-1, MDR1a, housekeeper GAPDH) was identified by real-time PCR. NOS activity was detected by conversion of [3H]-L-arginine to [3H]-L-citrulline and SOD activity was measured using UV VIS spectroscopy.ResultsWe observed a blood pressure elevation and decrease in NOS activity only after L-NAME application in both age groups. Gene expression of nNOS (youngs) and eNOS (adults) in the brain stem decreased after both inhibitors. The radical signaling pathway triggered by AT1R and p22phox was elevated in L-NAME adults, but not in young rats. Moreover, L-NAME-induced NOS inhibition increased antioxidant response, as indicated by the observed elevation of mRNA SOD3, HO-1, AT2R and MDR1a in adult rats. 7-NI did not have a significant effect on AT1R-NADPH oxidase-superoxide pathway, yet it affected antioxidant response of mRNA expression of SOD1 and stimulated total activity of SOD in young rats and mRNA expression of AT2R in adult rats.ConclusionOur results show that chronic NOS inhibition by two different NOS inhibitors has age-dependent effect on radical signaling and antioxidant/detoxificant response in Wistar rats. While 7-NI had neuroprotective effect in the brain stem of young Wistar rats, L-NAME- induced NOS inhibition evoked activation of AT1R-NAD(P)H oxidase pathway in adult Wistar rats. Triggering of the radical pathway was followed by activation of protective compensation mechanism at the gene expression level.Electronic supplementary materialThe online version of this article (doi:10.1186/s12929-017-0366-4) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Age-dependent redox status in the brain stem of NO-deficient hypertensive rats

et al. 2017

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“…In one of them, such effects are the consequence of hidroperoxide decomposition (d'Ischia et al, 2000). In the other one, L-NAME decreases glutathione peroxidase activity in the brain and increases markers of lipid peroxidation (Yargicoglu, et al, 2004). Also, in suboptimal arginine and tetrahydrobiopterine concentration (a cofactor for NOS activity), NOS syntheses hydrogen peroxide and reactive oxygen species (Rengasamy, et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Total anesthesia, rats brain surgery, nitric oxide (NO) and free radicals

Ankica¹,

Marina²,

Ninković³

et al. 2005

Acta vet. (Beogr.)

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It is expected that clinical recovery after surgically induced brain trauma is followed by molecular and biochemical restitution. Seven days after surgery, we investigated whether the plastic cannula implanted in the left brain ventricle of adult Wistar rats (n = 6-7), performed in pentobarbital anesthesia, could influence oxidative stress elements (superoxide anion and lipid peroxidation), as well as the antioxidative system (superoxide dismuthase-SOD). Also, we investigated whether nitric oxide (NO) is involved in these processes. Biochemical analyses was performed in the forebrain cortex, striatum and hippocampus. Clinical recovery was complete seven days after surgery. Thereafter, thirty minutes before decapitation, through the cannula, one group of rats received saline intracerebroventricularly (control group), and the treated group received Nω-nitro-L-arginine methyl ester (L-NAME). The third group was left unoperated and untreated. Before and after the treatments, rectal body temperature was measured. Compared to the untreated group the index of lipid peroxidation was increased in all three brain structures in the group that received saline (p<0.05 to 0.01). Application of L-NAME deteriorated it in the striatum and hippocampus (p<0.01 compared to the both other groups), but the value in the forebrain cortex was similar to the untreated group. Supeoxide anion level was decreased in the L-NAME treated group only in the striatum (p<0.01 compared to control and untreated groups), but SOD was increased in the hippocampus compared to the saline treated group (p<0.05). Seven days after brain surgery in pentobarbital anesthesia, recovery of biochemical disturbances was not parallel to clinical recovery. Long lasting biochemical changes are rather the consequence of brain injury than to pentobarbital anesthesia. In this experimental model, NO had protective effects, acting against lipid per oxidation in the striatum and hippocampus, but not in the forebrain cortex i. e. NO involvement in the free radical processes strongly depends on the observed brain region

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“…In another study, L-NMMA showed no differences in mean arterial pressure (MAP) after 2 h compared to the placebo group [136]. N(G)-nitro-L-arginine methyl ester (L-NAME) North America, Asia Patients with cardiogenic shock; patients with septic shock [137,138] Asymmetric dimethylarginine (ADMA) Europe Possible use as a cardiovascular risk factor [139,140] N(G)-methyl-l-arginine hydrochloride Europe Used to restore the balance of vasomotor tone in patients with septic shock [141,142] 7-nitroindazole (7-NI) Europe, North America Anticonvulsive properties in seizure models in rodents [143,144] Aminoguanidine Asia…”

Section: Selected Nos Inhibitors and Their Role In Therapymentioning

confidence: 99%

“…NOS inhibitors and research conducted on them[134][135][136][137][138][139][140][141][142][143][144][145][146].…”

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confidence: 99%

Human Nitric Oxide Synthase—Its Functions, Polymorphisms, and Inhibitors in the Context of Inflammation, Diabetes and Cardiovascular Diseases

Król

Kępińska

2020

IJMS

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In various diseases, there is an increased production of the free radicals needed to carry out certain physiological processes but their excessive amounts can cause oxidative stress and cell damage. Enzymes play a major role in the transformations associated with free radicals. One of them is nitric oxide synthase (NOS), which catalyzes the formation of nitric oxide (NO). This enzyme exists in three forms (NOS1, NOS2, NOS3), each encoded by a different gene. The following work presents the most important information on the NOS isoforms and their role in the human body, including NO synthesis in various tissues and cells, intercellular signaling and activities supporting the immune system and regulating blood vessel functions. The role of NOS in pathological conditions such as obesity, diabetes and heart disease is considered. Attention is also paid to the influence of the polymorphisms of these genes, encoding particular isoforms, on the development of these pathologies and the role of NOS inhibitors in the treatment of patients.

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Effects of N‐nitro l‐arginine methyl ester (l‐NAME), a potent nitric oxide synthase inhibitor, on visual evoked potentials of rats exposed to different experimental stress models

Abstract: This study clearly indicated that lipid peroxidation may be one possible factor affecting VEP components.

Cited by 10 publications

References 46 publications

Age-dependent redox status in the brain stem of NO-deficient hypertensive rats

Age-dependent redox status in the brain stem of NO-deficient hypertensive rats

Total anesthesia, rats brain surgery, nitric oxide (NO) and free radicals

Human Nitric Oxide Synthase—Its Functions, Polymorphisms, and Inhibitors in the Context of Inflammation, Diabetes and Cardiovascular Diseases

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