Influence of nitric oxide donors and peroxynitrite on the contractile effect and concentration of norepinephrine

Shelkovnikov, S. A.; Merlic, Craig A.; Gonick, Harvey C.

doi:10.1016/j.lfs.2003.11.006

Cited by 9 publications

(7 citation statements)

References 31 publications

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“…The hypothetic CsA-induced formation, in our animal model, of NO-derived oxygen and/or nitrogen reactive species, such as the superoxide and peroxynitrite, would hypothetically explain some of the above CsA and Is-5-Mn effects. Actually, peroxynitrite formation is associated with several deleterious effects, namely in the vasculature (Muijsers et al, 1997) and, according to some authors, also causes oxidation and nitration of catecholamines, thus decreasing their concentrations (Daveu et al, 1997;Shelkovnikov et al, 2004). If demonstrated in the ventricle and aorta tissues, the increased NOderived peroxynitrite formation would explain the CsA effect on left ventricle and aorta catecholamine contents as well as the CsA-induced toxicity.…”

Section: Discussionmentioning

confidence: 98%

Effect of preventive and regressive isosorbide 5-mononitrate treatment on catecholamine levels in plasma, platelets, adrenals, left ventricle and aorta in cyclosporin A-induced hypertensive rats

et al. 2005

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Increased vascular reactivity associated with cyclosporin A (CsA)-induced arterial hypertension might result from increased vasoconstriction and/or decreased vasodilatation. The administration of organic NO donors could have beneficial effects by the NO-cGMP reposition, but there is the risk of sympathetic nervous system worsening by neuro-hormonal counter-regulation. We evaluate the effect of preventive and regressive (curative) isosorbide 5-mononitrate (Is-5-Mn) treatment on blood pressures and on plasma, platelets, adrenals, left ventricle and aorta norepinephrine (NE) and epinephrine (E) contents, assessed by HPLC, in CsA-induced hypertensive rats. Five rat groups were tested: control (orange juice), CsA (5 mg/kg/day) and Is-5-Mn (150 mg/kg/day, bid) groups were treated for 7 weeks; preventive group (Is-5-Mn + CsA): Is-5-Mn during 2 weeks plus 7 weeks of Is-5-Mn + CsA; regressive group (CsA + Is-5-Mn): CsA during 7 weeks plus 5 weeks of CsA + Is-5-Mn. The increased BP in the CsA group was prevented, but was not reverted, by concomitant Is-5-Mn treatment. In the CsA-treated rats, there was a noticeable decrease in left ventricle NE and E contents and aorta NE levels and a moderate increase in circulating catecholamines, without significant effect in the adrenals values. When Is-5-Mn was preventively used, the CsA-induced effect on left ventricle and aorta was prevented. Concomitantly, however, the plasma-platelet catecholamine balance was disrupted, accumulating NE in plasma, whereas E increased in aorta, mimic the single Is-5-Mn-treated group. In opposition, in the group used as regressive Is-5-Mn therapy, the adrenals contents were higher compared with the CsA-group and, simultaneously, the CsA-evoked effects on circulating, left ventricle and

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Section: Discussionmentioning

confidence: 98%

Effect of preventive and regressive isosorbide 5-mononitrate treatment on catecholamine levels in plasma, platelets, adrenals, left ventricle and aorta in cyclosporin A-induced hypertensive rats

et al. 2005

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“…For example NO and NDMA receptors are jointly responsible for the regulation of noradrenaline release [189]. However NO together with peroxinitrite may deactivate the release of noradrenaline [190,191] and be an activator of NDMA mediated neuropathology [192]. …”

Section: Consequences Of Activated Inflamma-tory and Oandns Pathwaysmentioning

confidence: 99%

Oxidative and Nitrosative Stress and Immune-inflammatory Pathways in Patients with Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS)

Morris¹,

Maes

2014

117

139

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Myalgic Encephalomyelitis (ME) / Chronic Fatigue Syndrome (CFS) has been classified as a disease of the central nervous system by the WHO since 1969. Many patients carrying this diagnosis do demonstrate an almost bewildering array of biological abnormalities particularly the presence of oxidative and nitrosative stress (O&NS) and a chronically activated innate immune system. The proposal made herein is that once generated chronically activated O&NS and immune-inflammatory pathways conspire to generate a multitude of self-sustaining and self-amplifying pathological processes which are associated with the onset of ME/CFS. Sources of continuous activation of O&NS and immune-inflammatory pathways in ME/CFS are chronic, intermittent and opportunistic infections, bacterial translocation, autoimmune responses, mitochondrial dysfunctions, activation of the Toll-Like Receptor Radical Cycle, and decreased antioxidant levels. Consequences of chronically activated O&NS and immune-inflammatory pathways in ME/CFS are brain disorders, including neuroinflammation and brain hypometabolism / hypoperfusion, toxic effects of nitric oxide and peroxynitrite, lipid peroxidation and oxidative damage to DNA, secondary autoimmune responses directed against disrupted lipid membrane components and proteins, mitochondrial dysfunctions with a disruption of energy metabolism (e.g. compromised ATP production) and dysfunctional intracellular signaling pathways. The interplay between all of these factors leads to self-amplifying feed forward loops causing a chronic state of activated O&NS, immune-inflammatory and autoimmune pathways which may sustain the disease.

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“…NO at this concentration does not destroy epinephrine at conditions present in human body. In a previous publication we have reported that peroxynitrite but not NO donors destroys norepinephrine (Shelkovnikov et al, 2004). Destructive effect of peroxynitrite on epinephrine was stronger than on norepinephrine.…”

Section: Discussionmentioning

confidence: 75%

“…and superoxide (O 2 . ), peroxynitrite (ONOO À ), to decompose catecholamines has been previously demonstrated (De la Breteche et al, 1994;D'Ischia and Costantini, 1995;Daveu et al, 1997;Ducrocq et al, 1999;Rigobello et al, 2001;Kuo et al, 2003;Takakura et al, 2003). Recently we showed that peroxynitrite but not NO donors destroys norepinephrine (Shelkovnikov et al, 2004). In the present study, we compared epinephrine concentration before and after incubation with NO donors or peroxynitrite, using an HPLC method.…”

Section: Introductionmentioning

confidence: 89%

Peroxynitrite but not nitric oxide donors destroys epinephrine: HPLC measurement and rat aorta contractility

Shelkovnikov¹,

Gonick²

2004

Life Sciences

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Influence of nitric oxide donors and peroxynitrite on the contractile effect and concentration of norepinephrine

Cited by 9 publications

References 31 publications

Effect of preventive and regressive isosorbide 5-mononitrate treatment on catecholamine levels in plasma, platelets, adrenals, left ventricle and aorta in cyclosporin A-induced hypertensive rats

Effect of preventive and regressive isosorbide 5-mononitrate treatment on catecholamine levels in plasma, platelets, adrenals, left ventricle and aorta in cyclosporin A-induced hypertensive rats

Oxidative and Nitrosative Stress and Immune-inflammatory Pathways in Patients with Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS)

Peroxynitrite but not nitric oxide donors destroys epinephrine: HPLC measurement and rat aorta contractility

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