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The mechanism of action of amphetamine in a dopamine neuron. Depletion of cardiac catecholamines by guanethidine was prevented by TM-10 (2,6-xylyl choline ether bromide) but not by cocaine. From caffeine and nicotine to cocaine and amphetamines, each vary widely in how amply they.
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The effects of these amines were restored by incubation of the atria with norepinephrine. Amphetamines interact with VMAT in vitro, leading some investigators to conclude that they act as non-substrate inhibitors that elevate cytoplasmic dopamine by simply blocking its accumulation into. Atria from rats whose cardiac catecholamines were depleted by guanethidine did not respond to tyramine or amphetamine. Isolated atria also failed to exhibit the usual cardiostimulant responses to tyramine and amphetamine after exposure to guanethidine in the absence of any reduction in their concentrations of catecholamines. At this time, catecholamine concentrations in the heart were not significantly altered. Administration of guanethidine to animals anesthetized with urethane produced hypotension, inhibited the pressor actions of tyramine and amphetamine, and potentiated the response to norepinephrine. The influence of guanethidine on responses of the blood pressure and isolated, atropinized atria of rats to tyramine and amphetamine was studied.