Decreased platelet nitric oxide synthase activity and plasma nitric oxide metabolites in major depressive disorder

Chrapko, Wendy; Jurasz, Paul; Radomski, Marek W.; Lara, Nathalie; Archer, Stephen L.; Mellédo, Jean-Michel Le

doi:10.1016/j.biopsych.2004.03.003

Cited by 170 publications

(101 citation statements)

References 55 publications

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“…In that study, administration of paroxetine resulted in an increase in plasma NOx levels after 8 weeks of administration. This is particularly interesting as we have also shown, in a separate study, that plasma NOx levels and platelet eNOS activity are extremely low in unmedicated MD patients without conventional CV risk factors (Chrapko et al, 2004). It has also been shown, by other researchers, that 6 weeks of paroxetine normalized increased platelet reactivity in MD patients (Musselman et al, 2000).…”

Section: Introductionmentioning

confidence: 54%

Alteration of Decreased Plasma NO Metabolites and Platelet NO Synthase Activity by Paroxetine in Depressed Patients

Chrapko

Jurasz

Radomski

et al. 2005

Neuropsychopharmacol

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Although major depression (MD) and cardiovascular disease (CVD) have been conclusively linked in the literature, the mechanism associating MD and CVD is yet undetermined. The purpose of this paper is to further investigate a potential mechanism involving nitric oxide (NO) and to examine the effect of the selective serotonin reuptake inhibitor paroxetine on NO production by both platelets and the endothelium. In total, 17 subjects with MD and 12 healthy controls (HCs) with no known history of cardiovascular illness completed the study. Paroxetine was administered to both the MD patients and HCs over an 8-week period, and then medication was discontinued. Blood samples were taken at various times throughout paroxetine treatment and after discontinuation. Plasma NO metabolite (NOx) levels were measured by a chemiluminescence method. Platelet endothelial NO synthase (eNOS) activity was examined through the conversion of L-[14 C]arginine to L-[ 14 C]citrulline. Data were analyzed using t-tests and a linear mixed effects model. Baseline levels of both plasma NOx and platelet NOS activity were significantly lower in subjects with MD compared to HCs. Throughout paroxetine treatment, plasma NOx levels increased in both HCs and MD patients. However, platelet eNOS activity decreased in HCs, while no statistically significant change was evidenced in MD patients. These data suggest that, in MD patients, decreased peripheral production of NO, a potential contributor to increased cardiovascular risk, is modified by administration of the antidepressant paroxetine.

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Section: Introductionmentioning

confidence: 54%

Alteration of Decreased Plasma NO Metabolites and Platelet NO Synthase Activity by Paroxetine in Depressed Patients

Chrapko

Jurasz

Radomski

et al. 2005

Neuropsychopharmacol

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“…11,22 Subjects with depression also have low levels of plasma and platelet NO. 23,24 The low systemic levels of NO have been postulated to be responsible for the increased risk of cardiovascular events observed in subjects with depression, 24 as NO produces vasodilatation.…”

Section: Discussionmentioning

confidence: 99%

Depression Is Associated With High Levels of C-Reactive Protein and Low Levels of Fractional Exhaled Nitric Oxide

Cepeda¹,

Stang²,

Makadia³

2016

J. Clin. Psychiatry

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“…Analysis of polymorphisms of nitric oxide synthases have not yielded any conclusive evidence for their involvement in the pathogenesis of major depression (Yu et al 2003;Reif et al 2006). In a small sample of 15 subjects with major depression, decreased plasma nitric oxide metabolite levels and platelet endothelial nitric oxide synthase activity were observed (Chrapko et al 2004). Conversely, however, increased nitric oxide metabolite levels in plasma were suggested to be associated with suicide attempt, especially in major depressive patients (Lee et al 2006).…”

Section: Nitrogenmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

226

126

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Biological markers for depression are of great interest to aid in elucidating the causes of major depression. We assess currently available biological markers to query their validity for aiding in the diagnosis of major depression. We specifically focus on neurotrophic factors, serotonergic markers, biochemical markers, immunological markers, neuroimaging, neurophysiological findings, and neuropsychological markers. We delineate the most robust biological markers of major depression. These include decreased platelet imipramine binding, decreased 5-HT1A receptor expression, increase of soluble interleukin-2 receptor and interleukin-6 in serum, decreased brain-derived neurotrophic factor in serum, hypocholesterolemia, low blood folate levels, and impaired suppression of the dexamethasone suppression test. To date, however, none of these markers are sufficiently specific to contribute to the diagnosis of major depression. Thus, with regard to new diagnostic manuals such as DSM-V and ICD-11 which are currently assessing whether biological markers may be included in diagnostic criteria, no biological markers for major depression are currently available for inclusion in the diagnostic criteria.

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Decreased platelet nitric oxide synthase activity and plasma nitric oxide metabolites in major depressive disorder

Cited by 170 publications

References 55 publications

Alteration of Decreased Plasma NO Metabolites and Platelet NO Synthase Activity by Paroxetine in Depressed Patients

Alteration of Decreased Plasma NO Metabolites and Platelet NO Synthase Activity by Paroxetine in Depressed Patients

Depression Is Associated With High Levels of C-Reactive Protein and Low Levels of Fractional Exhaled Nitric Oxide

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

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