Posted by Keith Talent on June 7, 2004, at 13:10:55
In reply to Re: Anyone tried Anafranil » Keith Talent, posted by Pluto on June 6, 2004, at 3:18:32
> Nortriptyline and desipramine, both works by inhibiting noradrenaline
Inhibiting reuptake or antagonising receptors?
> rather than the other main neurotransmitter involved in the case of depression that is serotonin.
THE other main neurotransmitter? What about all the patients who require dopaminergic agents to fully recover from a Major Depressive Episode?
> Reboxetine, a specific noradrenaline reuptake inhibitor has more pronounced action on erction even at lower doses.
Is there is any scientific research supporting this assertion (that "reboxetine ... has more pronounced action on erction" than desipramine and/or nortriptyline)?
> Alpha 2 antagonism usually leads to better erections in man and in extreme cases priapism can occur. Almost all alpha 2 antagonists have priapism as a side effect, though this drug induced priapism doesn't usually lead to permenant sexual dysfunction. (Trazodone is an exception, which can cause treatment resistant priapism and consequently permenant erectile dysfunction).
I'm too lacking in knowledge of psychopharmacology to know anything about the validity of the above statements re alpha-2 antagonism and erectile function. But how is alpha-2 antagonism relevant to clomipramine, desipramine, nortriptyline or reboxetine?
> Clomipramine's high affinity on serotonin
Do you mean affinity for the serotonin transporter or for one or more serotonin receptors?
> is doubtlessly proved and it is this preciousness that makes it the most effective anti-OCD medication. This doesn't mean it doesn't possess other properties too.
Pluto, I'm glad that we agree on some things!
> Remember sertraline is a selective serotonin re-uptake inhibitor, but has pronounced dopaminergic actions too at doses higher than 100mg
Actually, I used to sort of believe this, but when you consider how high a concentration in the brain of sertraline (compared to the concentration produced by typically used doses) that you would need to cause a useful occupancy rate of dopamine transporters (say 70%-80%), and the daily dose needed to achieve such a concentration, and the basically 100% blockade of serotonin transporters that such a concentration would cause (with all the attendant side effects), then in practical terms sertraline does NOT have "pronounced dopaminergic actions too". I can't remember the exact ratio of potencies of sertraline at serotonin reuptake inhibition compared to dopamine reuptake inhibition, but I think it's around 10 000. My knowledge of pharmacology is insignificant, such that I don't know whether you can simply multiply the 10 000 by the typical 100 mg daily dose to arrive at a "dopaminergically effective" dose, but such a dose would have to be at least one gram per day, and perhaps ten or 100 grams. The side effects (and even the cost) of such doses would be intolerable.
> Clomipramine's affinity on noradrenaline
Again, affinity for the noradrenaline transporter and/or receptors?
> Peripheral vasodilation on both resistance vessels and capacitance vessels does not provoke reflex tachycardia, but can be beneficial in some cases of tachycardia.
Interesting. You learn something new every day. Does alpha-1 antagonism have greater vasodilatory effects on resistance or capacitance vessels? Also, do you accept that anticholinergic activity is, in large measure, responsible for the tachycardia caused by tricyclic antidepressants? It's a pleasure to converse with such an educated person. May I ask your educational and occupational backgrounds? As for myself, I quit med school and am doing a finance major (but am at Pyscho-Babble for the usual - personal health - reasons).
Thanks for your time,
Keith.
poster:Keith Talent
thread:353222
URL: http://www.dr-bob.org/babble/20040602/msgs/354545.html