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Cacti (mescaline containing) and Pindolol/Visken

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Xaratoostrah

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Mar 15, 2007
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I am going to start this topic assuming that most members in here are familiar with the readind material "On phenethylamines and Potentiation" and with Strassmans work "DMT the spirit molecule" ,where pindolol is said to act on 5HT1A receptors.Most psychedelics act both on 5HT1a receptors and 5HT2a receptors where it is thought that they owe their psychedelic action.

Mescaline is a psychedelic which is thought to act mostly on 5HT2a receptors leaving the 5HT1a subtype almost untouched from what i gather reading on its pharmacology.Maybe this is why it is in normal doses described as "gentle" and not as immersive as psilocybin.

So the question that comes to mind is what would happen if we gave mescaline an 5HT1a "component" in the experience? If ,that is ,instead of affecting only the 5HT2a receptors we somehow made it to affect 5HT1a also. Would the experience seem closer to psilocybin? Would the mescaline experience be enhanced (not "potentiated" per se) exhibiting new features previously nonexistent in the mescaline experience?

Such an endeavor ,that is altering the molecule to do this, would require some work,bot studying receptor affinities and designing a new molecule/synthesizing it and trying it.

Instead of this one could add this extra 1a action by coadministering a regular mescaline dose one is familiar with ,alongside with some Visken (pindolol) for example a single 5 mg Visken pill. Visken is quite accesible,not hard to find.

Has anyone tried anything like that? Has anyone got any pindolol and would be willing to try this experiment?

I would be very interested to hear your opinions,that why i ask.Maybe if pindolol is coupled with mescaline it could give an interersting experience
 
If ,that is ,instead of affecting only the 5HT2a receptors we somehow made it to affect 5HT1a also. Would the experience seem closer to psilocybin?
Click to expand...

afaik psilocybin's psychedelic effects are almost exclusively mediated through the 5ht2a receptor system. so a mescaline based 5ht1a agonist would not automatically be more similar to a psilocybin experience.

iea- and pea-based psychedelics are fundamentally different, even if they act on the same receptor and share many similarities (see here).
 
Ah thanks for the reply i have actually seen this discussion which i consider it being a very good analysis on the pharmacology of it all.

So pindolol would potentiate the experience so it seems... Has anyone heard of anyone trying the Pindolol-Mescaline combination?
 
I know buspirone has something to do with the 5HT1a receptor as it has a rolw in anxiety like responses, but I'll need to refreas my memory as to whether it's an agonist/antagonist/partial thingy

Pindolol, it's an 5HT1a antagonist? (spot lazy person!)
 
Yes FNB, its an 5HT1a antagonist. In some sources i have seen it reffered as a partial antagonist although im not sure...

Strassmans comments look promising ,dont they?
 
They do actually - being able to make PEA experiences more tryptamine like, giving a 'spectrum' of psychedelic experience.

Only thing is, I thought psilocin etc were 5HT1a agonists, not antagonists (best check, memory isn't infallable - even often mistaken in my case!)
 
actually i never tried one of the new benzodifuranyl compounds but i think they might be a good starting point for more tryptamine like peas.

can strassmans comments be found online? if so link please.
 
SWIM today put his guinea pig costume on and after taking 35gr of dried peruvianis he took a single tablet of 5mg pindolol(visken).He has found that this is indeed a very pleasurable combination. Nothing is taken away from mescaline's clarity but also it has been enhanced with general warming feeling. Overall effects are clearly amplified. But still should watch the effects on water metabolism because visken is a angio medicine. Highly recommended for the other people with similiar costumes.
 
Most interesting!!!

Since my interest has peaked i cant help but issue some questions.

Whats was the timeline of the administration? That is ,from what you say is apparent that SWIM took the pindolol after the cactus material but how long after?

Can you also give a more detailed account on qualitative and quantitative changes? Do you think the experience was potentiated quantitatively? What were the differences in the visual department and what on the mental effects? Did the experience last longer than usual? Anything other of note?
 
I'll be happy to tell you as much as I could understood. First SWIM has taken the pindolol around 4-5 hours fter ingestion of cactii so it was peak/after peak time. It's effects have definetely qualitatively increased especially emotional intensity was very pronounced. More or less it was like SWIM's psychedelic tolerance has vanished. It was blissfull and scary. Wheras a previous piracetam and mescaline combination was very visual oriented this combination was clearly not as good in that respect. SWIM personally does not like piracetam combination and says that it triggers bad trip and some nausea.

Again with harmaline addition mescaline's effects tend to center (ego becoming more dominant, almost having a sober mind).But with this combination ego was not so present, thoughts was easily going here and there. There was a lot relaxation in breathing and chest loosening. Lots of chi movements at lower and upper back. So I believe that it was healing. But the day after SWIM has noticed decreased urination and a lot of shivering. Which was the opposite of harmaline combination in which body and especially chest felt warmer and general mood was better. So for the duration of the trip pindolol, afterwards harmaline yielded better results.

With pindolol(visken) madness was more present, I can almost say that harmaline makes tripping shallow in SMIM's experience. But BOTH of them clearly extended the duration of the trip. (almost around 14-16 hours!!!)

I wonder why harmaline is such a revered chemical and said to be "the medicine" ???

Note: Pindolol seems to effect "after-psychedelic-sleep" badly therefore later that week general sleep quality has decreased noticably. (waking up very tired and sleepy). I wonder if this is due to REM changes ? these chemicals might change the way these cycles operates???
 
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It gets more interesting with every post,i think.

If you plan on trying this again ,try it with adding the pindolol at the start,that is take the pindolol at the same time you get the cacti. This would let you observe if it changes onset character/onset time plus it may provide for something completely different since last time you tried it you took it well int o the experience.

Same with harmaline i wonder what are the effects if one takes harmaline before and if one takes harmaline during the experience...
 
Interesting thread (needs to be resurrected) ... so pindolol enhances mescaline and DMT?

I guess that makes sense under the assumption that 5-HT1A receptors act in opposition to 5-HT2A. Blocking 1A decreases the hyperpolarizing influence of the 1A receptors, thereby releasing inhibition of 2A neurons. There must be some constitutive activity for mescaline to be enhanced as well ... probably not so simple though.

I'm curious how this would change the character of the experience. Anyone else have experience with this?

Also, the combination of buspirone with a dual 5-HT2A/1A agonist is interesting. I'm sure someone has tried this ... maybe PD would be a better place to get a response.

Buspirone is a partial agonist, but with low intrinsic efficacy. I would think that it would have more dramatic effects on the nature of tryptamine experience.
 
Buspirone belongs in one place only: the garbage bin, preferably where no living creature can accidentally ingest that poison. I believe I've taken it with one psychedelic or another (a phenethylamine I assume) and all it did was dull the trip significantly. Sorry I don't have any details, this was many years ago.

Just my 2c.
 
FnB: I think what you were trying to say ('spectrum' psychedelic idea) is probably not quite neurochem-/psychopharm- accurate.

The 5-HT1a mediated effects are not the result of displacing 5-HT at a post-synaptic membrane, but from the action on autoreceptors (which are usually activated by NT released from its own neuron, both near the synaptic terminal altering neurotransmitter release AND somatically+axonally, where they modulate probability of AP).

This also means that there are probably a whole wide array of compounds that can alter and potentiate the 5-HT2a agonists other than just the MAOIs. Has any played with drugs that have strong effects on mediating 5-HT activity presynaptically, such as w/ alpha2 adrenergic activity, as there is a major modulatory NE pathway from Locus coeruleus to the Raphe N.)

ps - Does anyone still have the reference for the paper which proposed that 5-HT2A activity was necessary but not sufficient for psychedelic activity (needed to cause phospholipase C activity or something)
 
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