There might be some regulation but the beauty of SR1 activity is that it seems only to affect pathological states. "The fire truck only leaves the station when there's fire." Hence the spectacularly low adverse effects for a CNS drug.
My theory is that SR1 activity seems to act like a high pass filter or overflow basin, only buffering the peaks of detrimental pathological cellular activity, whatever that maybe (ROS, Ca2+, ATP, Inflammation).
I remember that there was data available that A2-73 lowers AD related high blood pressure but not non-AD high blood pressure, which could make a case for a possible Ca2+ dependent mode of action. But also demonstrates inactivity in absence of pathological conditions.
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