Actually, while I've not looked at the Ki value for LSD at 5HT2b just lately, I'd hazard an educated guess that it would be one of the worse psychedelics for 5HT2b agonist effect.
Ergoloids in general often have very strong 5HT2b agonist properties. Not just acid, but ergoloid derivatives such as the dopamine agonist bromocriptine, used for parkinson's disease. I take a DA agonist myself, although for RLS not parkinson's, pramipexole, I said at the time that I specifically, wanted it to be a non-ergot alkaloid derivative, because of this. And while it might have nootropic effects, hydergine is one I've always left off the list of ones I'm willing to try. Well, I'd be willing to try it on an acute basis to explore it, but I wouldn't take it regularly, or any other ergot alkaloid derivative. Or things like ergotamine for migraines, if I had migraines (I'd be stockpiling it until I had a gram or two of ergotamine tartrate though, so I could whip out the diethylamine, prepare some phosphorus oxychloride, or nab myself one of the latest in peptide coupling reagents. Hell, bugger the diethylamine, I think I'd go for something more unusual, split the supplies between say, the morpholide, the dimethylazetidide, and a few others, since acid is already out there, that logically means it makes more sense to make something far rarer that'll not be found on the street.)
But, as a rule, ergot alkaloids tend towards very often being potent and long lasting 5HT2b agonists.
As far as taking an antagonist with it, a peripherally selective one, who knows the risks of that. 5HT2b is quite plainly important in controlling proliferation of cardiac fibroblasts, so too little activity could well be as problematic as too much. it'd be highly experimental to say the least, and to get results worth a damn as a study, it would need people to volunteer to take potent, long lasting 5HT2b agonist drugs on a regular basis to put themselves at risk of cardiac fibrosis and mitral valvulopathy, and to take a 5HT2b antagonist first (assuming its a competitive antagonist of course, not sure if 5HT2b has allosteric regulatory sites that would allow for uncompetitive and noncompetitive antagonism), and undergo regular ultrasonography to see if they develop cardiac fibrosis and mitral valve issues. And to be thorough, both positive and negative controls would have to be done, dosing another group of volunteers with only the 5HT2b agonist regularly, one on an inactive placebo, and a third control group taking solely the antagonist.
It's certainly no study that'd ever get approved by any regulatory ethics committee.
