Sorry to bump an old thread but I posted a similar thread not too long ago and this is something I have been looking into lately.
As endotropic said; LSD is a D2 receptor agonist. I must mention though that no other classical psychedelic has demonstrated such significant dopaminergic activity as LSD. I would imagine that by extension, AL-LAD and ALD-52 would probably have a similar effect.
LSD is definitely a very unique psychedelic. It's an ergoline. Prescription ergolines such as lisuride, cabergoline, bromocriptine and pergolide are powerful prolactin inhibitors so I wouldn't be surprised if LSD shared this quality to a certain extent.
Did you know that LSD also increases serum hGH?
Interestingly; studies have shown that mescaline (which is a phenethylamine) increases both serum hGH and prolactin. Now given mescaline's resemblance to dopamine and the fact that straight-up phenethylamine and amphetamine (alphamethylphenethylamine) both increase serum hGH and lower serum prolactin; one would expect the same from their psychedelic counterparts. Apparently this is not the case.
DMT and psilocin (which are tryptamines) on the other hand have been shown to raise serum prolactin but not hGH.
My theory is that increased prolactin is an inherent side effect of psychedelic 5HT agonism (this would offset any prolactin-inhibiting potential of mescaline's nature as a PEA). I think this sounds reasonable, as serotonin itself actually stimulates prolactin and cortisol release.
If we take a look at mescaline, phenethylamine and amphetamine; it also seems that increased growth hormone release is an inherent side effect of phenethylamine compounds.
I attribute LSD's prolactin-inhibiting qualities to the fact that it's an ergoline. I don't think any known psychedelic that isn't an ergoline has this kind of activity.
