PMID- 10486651
OWN - NLM
STAT- MEDLINE
DCOM- 19991022
LR  - 20221207
IS  - 0003-9683 (Print)
IS  - 0003-9683 (Linking)
VI  - 92
IP  - 8
DP  - 1999 Aug
TI  - [Reduction of the pressor effect of fluoxetine after V1A-vasopressin receptor 
      blockade in the conscious rats].
PG  - 985-9
AB  - Pharmacovigilance data have reported some cases of arterial hypertension in 
      patients treated with serotonin reuptake inhibitors. This side effect is now 
      called serotonin syndrome. Moreover, some authors have shown that these drugs 
      could reduce, at least in part, the fall in blood pressure (BP) observed in 
      experimental models or in human forms of orthostatic hypotension, suggesting a 
      modulation of the autonomic nervous system by these drugs. These data led us to 
      study in freely moving Wistar rats the mechanisms involved and the putative 
      involvement of autonomic nervous system. Intracerebroventricular (i.c.v.) 
      administration of fluoxetine (5-50 micrograms) induced an increase in BP similar 
      to which was obtained following central administration of serotonin (5-HT) (0.5-5 
      micrograms). After 5-HT, the pressor effect was immediate (1 min following 
      injection) and involved the baroreflex pathway (bradycardia). The 
      fluoxetine-induced pressor response reached its maximal 1 hour after injection 
      without any significant change in heart rate (HR). At the dose of 10 micrograms 
      i.c.v., fluoxetine significantly increased mean BP by 16 +/- 4 mmHg. This pressor 
      response was partially but significantly reduced by a pretreatment by the alpha 
      1-adrenoreceptor antagonist, prazosin (500 micrograms.kg-1 i.v.) (+7 +/- 4 mmHg, 
      p < 0.05) or by a V1A-vasopressin receptor antagonist (20 micrograms.kg-1 i.v.) 
      (+5 +/- 3 mmHg, p < 0.05). However, pretreatment by the beta-adrenoreceptor 
      antagonist, propranolol (1 mg.kg-1 i.v.) and the antagonist 5-HT2, ketanserine (5 
      mg.kg-1 i.v.) did not modify the fluoxetine-induced pressor response. In freely 
      moving rats receiving fluoxetine (10 micrograms i.c.v.), vasopressin plasma 
      levels were significantly higher (+39 +/- 5 pg.mL-1) than in rats receiving 
      saline (100 microL i.c.v.) (+14 +/- 4 pg.mL-1), thus confirming the involvement 
      of vasopressinergic mechanisms in the fluoxetine-induced pressor response. These 
      data suggest that in freely moving Wistar rats, central acute administration of 
      fluoxetine induces a pressor response mediated by both an increase in sympathetic 
      tone and a vasopressin release. This observation could suggest the putative use 
      of alpha 1-adrenoreceptors antagonists and/or V1A-vasopressin receptor 
      antagonists in the treatment of the serotonin syndrome.
FAU - Lazartigues, E
AU  - Lazartigues E
AD  - Laboratoire de pharmacologie medicale et clinique, INSERM U317, centre 
      Midi-Pyrenees de pharmacovigilance, de pharmaco-epidemiologie ets d'informations 
      sur le medicament, faculte de medecine, Toulouse.
FAU - Costes, S
AU  - Costes S
FAU - Brefel-Courbon, C
AU  - Brefel-Courbon C
FAU - Gharib, C
AU  - Gharib C
FAU - Tran, M A
AU  - Tran MA
FAU - Senard, J M
AU  - Senard JM
FAU - Montastruc, J L
AU  - Montastruc JL
LA  - fre
PT  - English Abstract
PT  - Journal Article
TT  - Reduction de l'effet presseur de la fluoxetine apres blocage des recepteurs V1A 
      de la vasopressine, chez le rat conscient.
PL  - France
TA  - Arch Mal Coeur Vaiss
JT  - Archives des maladies du coeur et des vaisseaux
JID - 0406011
RN  - 0 (Antidiuretic Hormone Receptor Antagonists)
RN  - 0 (Serotonin Uptake Inhibitors)
RN  - 01K63SUP8D (Fluoxetine)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - *Antidiuretic Hormone Receptor Antagonists
MH  - Autonomic Nervous System/drug effects
MH  - Blood Pressure/*drug effects
MH  - Fluoxetine/*antagonists & inhibitors
MH  - Injections, Intraventricular
MH  - Male
MH  - Rats
MH  - Rats, Wistar
MH  - *Selective Serotonin Reuptake Inhibitors
EDAT- 1999/09/16 00:00
MHDA- 1999/09/16 00:01
CRDT- 1999/09/16 00:00
PHST- 1999/09/16 00:00 [pubmed]
PHST- 1999/09/16 00:01 [medline]
PHST- 1999/09/16 00:00 [entrez]
PST - ppublish
SO  - Arch Mal Coeur Vaiss. 1999 Aug;92(8):985-9.