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Venlafaxine is a novel serotonin/noradrenaline reuptake inhibitor (SNRI) which has been shown clinically to be an effective antidepressant (AD) with a faster onset of action than serotonin specific reuptake inhibitors (SSRI). Preclinically, venlafaxine has been shown to potently inhibit dorsal raphe neuronal (DRN) firing through a 5-HT1A mediated mechanism, in a similar manner to SSRIs. Here we demonstrate the acute neurochemical effects of venlafaxine on extracellular concentrations of 5-HT and noradrenaline (NA) from the rat frontal cortex using in vivo microdialysis. Administration of venlafaxine (3-50 mg/kg s.c.) resulted in a significant dose-dependent increase in extracellular NA, but produced no significant increase in 5-HT concentrations. Combination treatment with the selective 5-HT1A antagonist WAY100635 produced a dose-dependent augmentation of venlafaxine-induced (3-30 mg/kg s.c) extracellular 5-HT concentrations, but had no further effect on NA above that produced by venlafaxine alone. WAY100635, at doses as low as 0.03 mg/kg s.c., maintained this potentiation effect. The beta-adrenergic/5-HT1A receptor antagonist (+/-)pindolol and the selective 5-HT1B/D antagonist GR127935 produced no significant augmentation of venlafaxine-induced changes in either 5-HT or NA. Using the alpha1 and alpha2-adrenoceptor antagonists, prazosin and idazoxane, we also demonstrate the role of the alpha-adrenoceptors in the augmentation of venlafaxine-induced changes. The possible mechanisms underlying venlafaxines improved clinical AD action and the potential for further enhancement of this SNRIs clinical effects are discussed.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10462128&dopt=Abstract

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J Auton Pharmacol. 1999 Apr;19(2):109-13.
Effect of venlafaxine hydrochloride in different preparations of isolated guinea-pig and rat organ tissues.

Velasco A, Arruza A, Maroto M, Carvajal A, Fernandez del Busto E, Garcia del Pozo J.

Department of Pharmacology, Faculty of Medicine, University of Valladolid, Spain.

A study was undertaken to know better the effects of venlafaxine hydrochloride on the responses of isolated rat vas deferens to noradrenaline and dopamine, those of isolated rat uterus to serotonin and histamine, and those of isolated guinea-pig ileum to acetylcholine and histamine. Venlafaxine hydrochloride increased the response of rat vas deferens to noradrenaline but not to dopamine. Venlafaxine did not alter the response of rat isolated uterus to serotonin. In rat uterus, venlafaxine did not modify the response to histamine but was able to increase it in guinea-pig ileum. An anticholinergic effect was observed with the lowest concentration tested. Although venlafaxine is a selective serotonine reuptake inhibitor in the central nervous system, serotonin uptake was not seen in the rat uterus. The anticholinergic effects observed in the present study might be consistent with some of the side-effects associated with venlafaxine.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10466944&dopt=Abstract

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J Pharmacol Exp Ther. 1999 Oct;291(1):280-4.
Mechanism of sodium channel block by venlafaxine in guinea pig ventricular myocytes.

Khalifa M, Daleau P, Turgeon J.

Quebec Heart Institute, Laval Hospital, Faculty of Pharmacy, Laval University, Sainte-Foy, Canada.

Venlafaxine is a newly introduced antidepressant agent. The drug causes selective inhibition of neuronal reuptake of serotonine and norepinephrine with little effect on other neurotransmitter systems. Cases of seizures, tachycardia, and QRS prolongation have been observed following drug overdose in humans. The clinical manifestations of cardiac toxicity suggest that venlafaxine may exhibit cardiac electrophysiological effects on fast conducting cells. Consequently, studies were undertaken to characterize effects of venlafaxine on the fast inward sodium current (I(Na)) of isolated guinea pig ventricular myocytes. Currents were recorded with the whole-cell configuration of the patch-clamp technique in the presence of Ca(2+) and K(+) channel blockers. Results obtained demonstrated that venlafaxine inhibits peak I(Na) in a concentration-dependent manner with an estimated IC(50) of 8. 10(-6) M. Inhibition was exclusively of a tonic nature and rate-independent. Neither kinetics of inactivation (tau(inac)= 0.652 +/- 0.020 ms, under control conditions; tau(inac)= 0.636 +/- 0.050, in the presence of 10(-5) M venlafaxine; n = 5 cells isolated from five animals) nor kinetics of recovery from inactivation of the sodium channels (tau(re)= 58.7 +/- 1.6 ms, under control conditions; tau(re)= 54.4 +/- 1.8, in the presence of 10(-5) M venlafaxine; n = 10 cells isolated from six animals) were significantly altered by 10(-5) M venlafaxine. These observations led us to conclude that venlafaxine blocks I(Na) following its binding to the resting state of the channel. Thus, the characteristics of block of I(Na) by venlafaxine are different from those usually observed with most tricyclic antidepressants or conventional class I antiarrhythmic drugs.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10490914&dopt=Abstract

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