Plasma Levels of Catecholamine Metabolites Predict the Response to Sulpiride or Fluvoxamine in Major Depression

Ueda, Nobuhisa; Yoshimura, Reiji; Shinkai, Koji; Nakamura, Jun

doi:10.1055/s-2002-34116

Cited by 41 publications

(34 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This might explain why in our study depressed patients with the highest BPV responded strongest to selective noradrenergic treatment with reboxetine. Our data comply with previous reports showing that high plasma noradrenaline [2] , high plasma levels of the noradrenaline metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) [24] and enhanced pineal gland production of melatonin, a measure that refl ects increased noradrenergic function [25] , seem to be associated with good outcome in major depression. The relationship between noradrenergic dysfunction and antidepressive treatment response was also investigated in other studies.…”

Section: Discussionsupporting

confidence: 92%

Basal Prolactin Values Correlate with Response to Reboxetine Treatment in Major Depression, but Not with Response to Citalopram

Moeller¹,

Hetzel²,

Michael³

et al. 2005

Neuropsychobiology

View full text Add to dashboard Cite

Little is known about variables that might predict outcome in major depression. Recently, basal prolactin values (BPV) have been suggested to predict response to treatment with tricyclic antidepressive drugs. In order to examine whether BPV predict response to selective mono-aminergic therapy, 24 in-patients with major depression were treated in a single-masked, randomised study using the most selective noradrenergic or serotonergic reuptake inhibitors available for antidepressant treatment, i.e. reboxetine and citalopram. A significant correlation between BPV and treatment response to reboxetine was found, but not between BPV and response to citalopram. As BPV are influenced by noradrenergic activity, it can be hypothesized that depressed patients with comparatively high BPV have a relatively high noradrenergic function. This might explain why in our study depressed patients with the highest BPV responded strongest to selective noradrenergic treatment with reboxetine. As measurement of BPV is simple, further studies are suggested to examine the possible clinical value of the link between prolactin, noradrenergic function in major depression and treatment response.

show abstract

Section: Discussionsupporting

confidence: 92%

Basal Prolactin Values Correlate with Response to Reboxetine Treatment in Major Depression, but Not with Response to Citalopram

Moeller¹,

Hetzel²,

Michael³

et al. 2005

Neuropsychobiology

View full text Add to dashboard Cite

show abstract

“…10, [36][37][38] While our reported fluvoxamine IC 50 value for the inhibition of Kv channels was higher than the reported therapeutic plasma concentration, significant Kv channel inhibition was observed at lower concentrations of 0.3 and 1 µM (Fig. 2).…”

Section: Discussionmentioning

confidence: 63%

The Effects of the Selective Serotonin Reuptake Inhibitor Fluvoxamine on Voltage-Dependent K<sup>+</sup> Channels in Rabbit Coronary Arterial Smooth Muscle Cells

Hong

Kim

et al. 2015

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

We demonstrated the inhibitory effect of fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), on voltage-dependent K (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells using a whole-cell patch clamp technique. Fluvoxamine reduced the amplitude of Kv currents in a concentration-dependent manner with an IC 50 value of 3.71 1.09 µM and a Hill coefficient of 0.62 0.14. Although fluvoxamine did not significantly affect the steady-state activation curve, it shifted the steady-state inactivation curve toward a more negative potential. Pretreatment with another SSRI, paroxetine, did not affect the basal Kv current and did not alter the inhibitory effect of fluvoxamine on Kv channels. We concluded that fluvoxamine inhibits the Kv current in a concentration-dependent manner and in a closed (inactivated) state of the Kv channels independent of serotonin reuptake inhibition.Key words fluvoxamine;voltage-dependentK + channel; coronary artery; smooth muscle; selective serotonin reuptake inhibitorFluvoxamine is a selective serotonin reuptake inhibitor (SSRI) that has been used for the treatment of major depression, anxiety, and panic disorder since 1983 in many countries, including those in Europe and Japan.1,2) The antidepressant activity of fluvoxamine is derived from inhibition of serotonin reuptake in the central nervous system with negligible effects on other neurotransmitter reuptake systems.3,4) A recent study indicated that fluvoxamine showed high affinity for the σ1 receptor, which has a neuromodulatory role on the neurotransmitter system and an antidepressant-like effect. 5-7)Although fluvoxamine has beneficial effects in the treatment of depression, its administration is associated with common side effects, including nausea, anorexia, palpitations, headache, and dizziness. 8)Fluvoxamine also affects ion channels, such as the human ether-a-go-go related (hERG) K + and Kv1.5 channels. 9,10) However, these studies were performed primarily in cultured cell lines rather than in native cells. Therefore, questionsremainabouttheeffectoffluvoxamineonionchannels from freshly isolated cells, particularly vascular smooth muscle cells. 11,12) Our previous reports suggested that Kv channels participate in the regulation of resting membrane potential and thus resting tone in some arteries. 13,14) In addition, pathological states such as hypertension, diabetes, and hypoxia, are closely related with alteration of Kv channel activity and expression in the vasculature.15) Therefore, the adverse effects of drugs on Kv channels should be clearly determined to correctly interpret experimental data regarding vascular disorders.Considering the usefulness of fluvoxamine as a SSRI and the physiological importance of Kv channels, the effects of fluvoxamine on vascular Kv channel should be clearly examined to avoid toxic effect on the vasculature when applying fluvoxamineasantidepressantdrug.In the present study, we investigated the effects of fluvoxamine on Kv channels using freshly isolated coronary ...

show abstract

“…Fluoxetine has been shown to normalize plasma levels of norepinephrine metabolites in patients affected by panic disorders [14] . Plasma levels of catecholamine metabolites may predict the response to fl uvoxamine in major depression [15] . A negative correlation has been observed between changes in plasma catecholamine metabolites and clinical response to paroxetine in depressed patients [16] .…”

Section: Introductionmentioning

confidence: 99%

Plasma Catecholamine Levels after Fluoxetine Treatment in Depressive Patients

Blardi

Lalla²,

Auteri³

et al. 2005

Neuropsychobiology

View full text Add to dashboard Cite

It is known that selective serotonin reuptake inhibitors, widely used as antidepressive drugs, act by inhibiting the cell reuptake of serotonin, but their effect on the catecholaminergic system is not yet completely understood. In this study, we investigated plasma concentrations of norepinephrine, epinephrine and dopamine after acute and chronic administration of fluoxetine in depressive patients. Twelve patients affected by major depression received a single oral dose of fluoxetine in the morning, 5 mg in the first 5 days, 10 mg from the 6th to the 10th day and 20 mg from the 11th to the 40th day. Twelve healthy subjects received a placebo under identical testing procedures. Blood samples were collected at baseline and 7, 10 and 24 h after drug administration on the 1st day of fluoxetine administration at a dose of 5 mg, and on the 1st and the 30th day of fluoxetine administration at a dose of 20 mg (days 11 and 40 of treatment, respectively). We found that plasma norepinephrine, epinephrine and dopamine levels significantly increased after acute and chronic treatment (p < 0.001), reaching the highest concentrations on the last day. No significant changes of these parameters were observed in control patients.

show abstract

Plasma Levels of Catecholamine Metabolites Predict the Response to Sulpiride or Fluvoxamine in Major Depression

Cited by 41 publications

References 34 publications

Basal Prolactin Values Correlate with Response to Reboxetine Treatment in Major Depression, but Not with Response to Citalopram

Basal Prolactin Values Correlate with Response to Reboxetine Treatment in Major Depression, but Not with Response to Citalopram

The Effects of the Selective Serotonin Reuptake Inhibitor Fluvoxamine on Voltage-Dependent K<sup>+</sup> Channels in Rabbit Coronary Arterial Smooth Muscle Cells

Plasma Catecholamine Levels after Fluoxetine Treatment in Depressive Patients

Contact Info

Product

Resources

About