Vascular sympathetic neurotransmission and its serotonergic regulation are modified by chronic fluoxetine treatment

Fluoxetine Treatment Decreases Cardiac Vagal Input and Alters the Serotonergic Modulation of the Parasympathetic Outflow in Diabetic Rats

“…After anaesthesia and pithing, fluoxetine treatment did not modify basal MBP and HR compared to FT normoglycaemic [ 25 , 30 ] and non-treated diabetic rats (current data, [ 19 , 20 , 27 ]). While most of the agonists and antagonists used in this work did not modify either MBP or HR, it is remarkable that all doses of 5-HT and α-methyl-5-HT induced increases in MBP that immediately restored to basal values as occurred in FT normoglycaemic animals [ 25 ].…”

“…In our experiments, alloxan administration induced, from day 2 after injection, a syndrome resembling human T1DM [ 19 , 20 , 28 ] that was confirmed by measurement of blood glucose levels. Our animals were chronically treated with the antidepressant fluoxetine, which increases extracellular serotonin levels [ 29 ] at a dose and period (10 mg/kg/day; 14 days) that originate levels in plasma similar to patients treated with therapeutic doses [ 25 , 27 , 30 , 31 , 32 ]. Our results reveal that chronic fluoxetine treatment significantly reduces blood glucose levels compared to diseased (alloxan) animals without treatment, even though glycaemia does not return to normal levels, as we have previously described [ 27 ].…”

Renal Sympathetic Hyperactivity in Diabetes Is Modulated by 5-HT1D Receptor Activation via NO Pathway

“…The serotonergic system plays a pivotal function in cardiovascular homeostasis, both by directly regulating blood vessel contraction and dilation in different vascular beds such as mesentery, hindquarters, and kidneys [ 14 , 15 , 16 ], or by indirectly modulating the vegetative nervous system at the vascular and cardiac levels [ 17 , 18 , 19 , 20 ]. In this sense, 5-HT causes rat vascular sympatho-inhibition mainly by activation of 5-HT 1D receptors [ 18 , 19 , 21 ].…”