Give me some help on my speculation here, please. Speaking specifically about the Alpha receptors, would one want to damp down the receptor response by using a antagonist? If so, then that would increase acetylcholine and norepinephrine, correct? Any spec speculation on what else an antagonist might do?
Yes, an antagonist should help in diminishing the up-regulation of the ADRA2A gene.
I started Yohimbe about two weeks ago, which is the most potent and specific antagonist of ADRA2A. I have chronically low norepinephrine, and was taking an NRI to deal with my orthostatic intolerance for the past year. When switching to Yohimbe, my OI stayed under control, plus I seem to have had no PEM, despite spending about 14 hours in airports and on an airplane.
Gut motility has also improved, to the extent that I had to cut back my magnesium, yet don't have any of the muscle twitching and such I'd usually get with less magnesium. Theoretically, it should also help with lipolysis, which can be suppressed by ADRA2A.
I haven't had any side effects thus far, and no signs of needing to increase my dosage. If anything, the effects seem to be more constant now, possibly due to norepinephrine levels rising in general? But its actions should be very specific for ADRA2A, ADRA2B, and ADRA2C, unlike the less powerful pharmaceutical ADRA2A antagonists, which also have a significant or even larger effect on a histamine receptor, HTP receptors, etc.