How could inhibiting the reuptake of epinephrine possibly be effective in the case of clinical anxiety?

I do not know the exact answer here. Most practitioners I'm aware of shy away from the use of noradrenergic drugs in the treatment of anxiety, and anecdotally they either work very well, or make things much worse. However, the NICE review states that they are effective, though it also has some other boneheaded statements in it.

When we generally think of epi or nor-epi, we think of their role in the sympathetic nervous system - fight or flight, the adrenaline rush, their vasoconstrictive properties. What's important to realize, is that as monamine transmitters that couple to GPCRs, they are not directly excititory, they are modulatory. Modulatory in the sense that they do not cause the direct depolarization of a membrane (AP firing or muscle contraction), but instead alter the internal metabolism of the cell, typically through cAMP (in the sympathetic NS)

One of the more recent discoveries is that of a small peptide transmitter called neuropeptide S. NPS, and it's receptor, NPSR, are localized almost exclusively to the locus coeruleus in the brain. This single area contains noradrenergic neurons that project to basically every meaningful area of the brain. Now, here's the strange part - activation of NPSR has two significant clinical effects in mouse models - potent anxiolysis on a par with benzodiazepines, and at the same time it promotes strong arousal/alertness. This is a contradiction to the MoA we normally associated with relief of anxiety - sedation.

There are several possibilities here. If I were to hazard a guess, I'd say that the LC's termination in the Amygdala is important with regards to norepi's relief of anxiety. One is that, the modulation norepi causes in the receiving neurons is not the same as what happens in, say a muscle innervated by the SNS. It could increase the threshold a nerve needs to fire, slowing down activity. Another possibility is that these norepi neuron projections could terminate on inhibitor neurons, say GABAergics, and further down the line cause inhibition.

There's also the possibility that there is a much higher level effect, such as say altering perception, or information processing. I don't regard this plausible without evidence to back it up - we're dealing with levels of the brain generally below that level of complexity. It's not impossible, just not likely given the above more mundane alternatives.

There's probably stuff I should be thinking of and am not, but this is the sort of thing that occurs to me at 1 AM.

...What you're saying would not scare me - i think of that's pathetic and tries to sound smart, while truly little or no of what you're saying makes lots experience. ...i don't comprehend how each and every individual can answer your question...we could desire to comprehend what it is, first. Your narrative is a tangled bunch of psychobabble. ...i'm specific you have not ridded your self of ideals, yet i will wager money you may not articulate them. ...Oh, and with the help of the way, i'm unfastened, i'm unfastened certainly. "If the Son instruments you unfastened, you're unfastened certainly." John 8:36 ...you may question all you desire - in case you desire peace, excitement, eternal existence, and Heaven certain - believe on the Lord Jesus Christ and be saved (Acts sixteen:31). ...I do desire you a blessed eternity in Heaven with Jesus. ...Whosoever will, could come.

the reason of anxiety hasnt been discoverd

but I think it can be effective on restlessness tension and dyspnea

but not effective on tachycardia