Allegedly one of the mechanisms of propranolol is inhibition of norepinephrine in the catecholaminergic system (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671824/#__sec15title)
Since the precursor to norepinephrine is dopamine, could this inhibition serve to retain dopamine in the CNS? If so, would this dopamine be active or would it be a false neurotransmitter (non-active)? Or would the inhibition of norepinephrine possibly occur elsewhere, before dopamine is even synthesized?
I ask since if the MOA involves blocking the breakdown of dopamine, it could theoretically help with adrenal fatigue given the lower concentration of norepinephrine and epinephrine, in addition to the excess dopamine helping in other ways to combat fatigue.
I'm more interested in the MOA specifically rather than the efficacy of propranolol since I have some other ideas to explore if the MOA is indeed different.
On another note I'm interested in the role a mutation leading to a less active dopamine beta-monooxygenas enzyme (enzyme involved in dopamine -> norepinephrine conversion) may play in terms of chronic fatigue and depression. All medical literature I can find behind the very rare deficiency of this enzyme seems to correlate with various clinical pathologies without mentioning any potential psychological benefits.
Since the precursor to norepinephrine is dopamine, could this inhibition serve to retain dopamine in the CNS? If so, would this dopamine be active or would it be a false neurotransmitter (non-active)? Or would the inhibition of norepinephrine possibly occur elsewhere, before dopamine is even synthesized?
I ask since if the MOA involves blocking the breakdown of dopamine, it could theoretically help with adrenal fatigue given the lower concentration of norepinephrine and epinephrine, in addition to the excess dopamine helping in other ways to combat fatigue.
I'm more interested in the MOA specifically rather than the efficacy of propranolol since I have some other ideas to explore if the MOA is indeed different.
On another note I'm interested in the role a mutation leading to a less active dopamine beta-monooxygenas enzyme (enzyme involved in dopamine -> norepinephrine conversion) may play in terms of chronic fatigue and depression. All medical literature I can find behind the very rare deficiency of this enzyme seems to correlate with various clinical pathologies without mentioning any potential psychological benefits.