• N&PD Moderators: Skorpio | thegreenhand

Extreme transpiration from venlafaxine (serotonin?)

Venlafaxine is an SNDRI..

You are correct about your last point. That is a hell of a lot of norepinephrine :/ I wouldn't want to be on that combo every day. It sounds fun to combine recreationally, though.



Propranolol or any beta blocker would only make the sweating worse. It's actually a common side effect of them. By blocking the beta adrenergic receptors, it leaves the alpha adrenergic receptors entirely unopposed, and they are free to be activated by norepinphrine and epinephrine. This isn't a good thing to recommend. The alpha blockers or alpha 2 agonists would be work.

The concentration of NE or E that binds to a receptor is negligible to the concentration of free, unbound molecules. In other words, blocking a ligand from binding to a receptor will barely result in more free ligands to activate other exposed receptors, in most cases. The phenomenon where this does occur is called ligand depletion, and it would only occur when you're dealing with an extremely potent ligand (probably with sub-picomolar affinity at least).
 
I've read a lot on ADD/ADHD forum and the general consensus is that NDRIs are generall unpleasant and have awful comedowns. Amphetamines seem to be always preferred.

But that seems to be contradicted when it comes to recreational drugs. Cocaine has quite a good reputation compared to methamphetamine for some reason even though amphetamine and methamphetamine are better/safer drugs.

Cocaine is a TRI, and probably not all of its recreational affects can be pinned down to DA reuptake inhibition. Its duration is also much shorter, which is in a lot of cases preferred in recreational situations.

Crack is more recreational because of the implications of its ROA.
 
Cocaine is a TRI, and probably not all of its recreational affects can be pinned down to DA reuptake inhibition. Its duration is also much shorter, which is in a lot of cases preferred in recreational situations.

Crack is more recreational because of the implications of its ROA.

It's a sodium channel blocker and sigma agonist as well.
 
Then why is sweating such a common side effect of beta blockers - typical of alpha activity, as well as hypertensive reactions?

This link mention unopposed alpha activity; it is a relevant action:

http://howmed.net/pharmacology/beta-adrenoceptor-blockers/

You can google other ones.

Through some other mechanisms (that may still result in increased alpha activation), but it definitely isn't due to ligand depletion. The number of ligand molecules is very significantly greater than the number of receptor molecules, and so when a receptor is prevented from being occupied by say an NE molecule, the total number of molecules available to bind to and activate other receptors goes up by a very very small proportion.
 
Venlafaxine is an SNDRI..

You are correct about your last point. That is a hell of a lot of norepinephrine :/ I wouldn't want to be on that combo every day. It sounds fun to combine recreationally, though.



Propranolol or any beta blocker would only make the sweating worse. It's actually a common side effect of them. By blocking the beta adrenergic receptors, it leaves the alpha adrenergic receptors entirely unopposed, and they are free to be activated by norepinphrine and epinephrine. This isn't a good thing to recommend. The alpha blockers or alpha 2 agonists would be work.

My bad if this is not what you were trying to get across.
 
The beta and alpha receptors have effects that slightly inhibit each other. By blocking beta receptors alpha receptors lose that inhibition and have a stronger action with the same amount of ligand binding
 
The beta and alpha receptors have effects that slightly inhibit each other. By blocking beta receptors alpha receptors lose that inhibition and have a stronger action with the same amount of ligand binding

They have slightly more ligand binding, since there is a little extra epinephrine to activate them as well.
 
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