Fluoxetine and nortriptyline affect NTPDase and 5′-nucleotidase activities in rat blood serum

Pedrazza, Eduardo Luiz; Senger, Mário Roberto; Rico, Eduardo Pacheco; Zimmermann, Fernanda Francine; Pedrazza, Leonardo; Sarkis, João José de Freitas; Bonan, Carla Denise

doi:10.1016/j.lfs.2007.08.020

Cited by 9 publications

(2 citation statements)

References 39 publications

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“…The most important mechanisms appear to be SSRI-induced inhibition of serotonin uptake in platelets resulting in decreased serotonin release from platelets in case of vascular injury with the consequence of diminished serotonin-triggered platelet aggregation and vasoconstriction (prolongation of bleeding time and reduced platelet aggregability and activity) [19,32,33]. However, other mechanisms such as SSRI-induced increase in gastric acid secretion that may exhibit ulcerogenic effects (as shown already in rodent models [34,35] and suggested by increased rates of first prescriptions of peptic ulcer drugs in patients receiving NSAID/SSRI compared to NSAID/non-selective antidepressant [36]) [19], SSRI-related pharmacokinetic interactions with the cytochrome P450 (CYP) enzymes (particularly regarding paroxetine, fluvoxamine, and fluoxetine) inhibiting the metabolisation of NSAIDs and antiplatelet drugs [19,37] as well as a possible influence of SSRI on other metabolic pathways involved in haemostasis [38] are discussed as well.…”

Section: Introduction ▼mentioning

confidence: 99%

Risk of Bleeding Related to Selective and Non-selective Serotonergic Antidepressants: A Case/Non-case Approach Using Data from Two Pharmacovigilance Databases

et al. 2014

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Signal detectioning in 2 pharmacovigilance databases suggest that serotonin reuptake inhibition is not associated with an increased risk of bleeding. However, underreporting may have accounted for the evaluated absent associations, particularly concerning SSRI. Regarding the detected increased risk of bleeding associated with hypericum, pharmacokinetic drug-drug interactions may be relevant independent of serotonin reuptake inhibition.

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Section: Introduction ▼mentioning

confidence: 99%

Risk of Bleeding Related to Selective and Non-selective Serotonergic Antidepressants: A Case/Non-case Approach Using Data from Two Pharmacovigilance Databases

et al. 2014

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“…Amitriptyline and desipramine, which are antidepressants that increase the availability of monoamines, displayed antinociceptive effects dependent of adenosine receptors activation [ 8 – 10 , 42 – 44 ]. In addition, antidepressants that increase the extracellular availability of monoamines seem to modulate nucleotide hydrolysis in the central nervous system (CNS), presenting stimulatory or inhibitory effect depending on the treatment duration and brain structure [ 45 – 47 ]. The effects of antidepressants on adenosine system seem to reflect increased availability of adenosine following an effect on transport and not necessarily effects on amine transporters [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Uliginosin B, a Possible New Analgesic Drug, Acts by Modulating the Adenosinergic System

Stolz

Costa

Medeiros

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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Uliginosin B (ULI) is a natural acylphloroglucinol that has been proposed as a new molecular scaffold for developing analgesic and antidepressant drugs. Its effects seem to be due to its ability to increase monoamines in the synaptic cleft by inhibiting their neuronal uptake without binding to their respective transporters, but its exact mode of action is still unknown. Considering the importance of the purinergic system to pain transmission and its modulation by monoamines availability, the aim of this study was to investigate the involvement of adenosinergic signaling in antinociceptive effect of uliginosin B. The selective adenosine A1 receptor antagonist DPCPX and the selective A2A antagonist ZM 241385 prevented the effect of ULI in the hot-plate test in mice. Pretreatment with inhibitors of adenosine reuptake (dipyridamole) or adenosine deaminase (EHNA) did not affect the ULI effect. On the other hand, its effect was completely prevented by an inhibitor of ecto-5′-nucleotidase (AMPCP). This finding was confirmed ex vivo, whereby ULI treatment increased AMP and ATP hydrolysis in spinal cord and cerebral cortex synaptosomes, respectively. Altogether, these data indicate that activation of A1 and A2A receptors and the modulation of ecto-5′-nucleotidase activity contribute to the antinociceptive effect of ULI.

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Purinergic Signaling in Depression

Ribeiro

Kaster

Ulrich

et al. 2023

Purinergic Signaling in Neurodevelopment, Neuroinflammation and Neurodegeneration

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Fluoxetine and nortriptyline affect NTPDase and 5′-nucleotidase activities in rat blood serum

Cited by 9 publications

References 39 publications

Risk of Bleeding Related to Selective and Non-selective Serotonergic Antidepressants: A Case/Non-case Approach Using Data from Two Pharmacovigilance Databases

Risk of Bleeding Related to Selective and Non-selective Serotonergic Antidepressants: A Case/Non-case Approach Using Data from Two Pharmacovigilance Databases

Uliginosin B, a Possible New Analgesic Drug, Acts by Modulating the Adenosinergic System

Purinergic Signaling in Depression

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