Plasma Catecholamine Levels after Fluoxetine Treatment in Depressive Patients

Abstract

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.

Effects of the Selective Serotonin Reuptake Inhibitor Fluoxetine on Counterregulatory Responses to Hypoglycemia in Individuals With Type 1 Diabetes

“…Similar to the findings in healthy humans, fluoxetine resulted in an increased response of cortisol during hypoglycemia. This also demon- strates that the SSRI was having effects to activate multiple neural pathways within the central nervous system (7). Accompanying the amplified SNS responses were significant increases in blood pressure and heart rate during hypoglycemia following fluoxetine.…”

Serotonin and histamine mediate gastroprotective effect of fluoxetine against experimentally-induced ulcers in rats

“…Fluoxetine markedly enhanced COX-1 expression, while ranitidine did not improve COX-1 in both models of ulcer induction. This could be explained by an ability of fluoxetine to increase plasma adrenaline (Blardi et al 2005) that, in turn, is able to increase COX-1 levels in gastric tissue by stimulating 2 receptors (Suleyman et al 2009b). The current results also showed that fluoxetine increased expression of COX-2 in both models, a finding in agreement with a previous study wherein fluoxetine up-regulated brain COX-2 expression (Wang et al 2011).…”

Effects of a Selective Serotonin Reuptake Inhibitor, Fluoxetine, on Counterregulatory Responses to Hypoglycemia in Healthy Individuals

“…The neural mechanisms responsible for fluoxetine's effects on amplifying counterregulatory responses to hypoglycemia are not evident from this study. Numerous studies have demonstrated interactions between serotonergic (both 5-HT1A and 5-HT3) and catecholamine neurotransmission pathways in multiple areas of the brain (8). These include forebrain (thalamus and hypothalamus) and hindbrain nuclei that are known to play important roles in regulating ANS responses during hypoglycemia.…”

“…However, although SSRIs are potent inhibitors of neuronal serotonin uptake, they also have the ability to block norepinephrine transport (7). This could increase sympathetic outflow activity (2,8). Baudrie and Chaouloff (9) have previously reported an increased hyperglycemic response to 2-deoxy-D-glycose in conscious rats following serotononergic receptor antagonists, implying increased counterregulation in these animals.…”