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drugs that induce a steady state of NE from the presynaptic neurons, bypassing normal processes. Affects all alpha and beta cells. The effect is the increase of adrenergic sympathetic activity.
drugs that mimic the action of NE at all adrenergic receptors in a non-selective manner
drugs that only bind to the alpha-1 NE receptors on target organs and act agonistically to NE
drugs that selectively bind to beta NE receptors and act agonistically to NE
non selective alpha NE receptor blockers block alpha 1&2 receptors. the overall effect is to increase the activity of adrenergic synapses with beta receptors, while diminishing activity of adrenergic synapses with alpha 1&2
drugs that selectively bind to beta-1 NE receptors on target organ cells and act agonistically as NE
drugs that selectively bind to beta-2 NE receptors on target organ cells and act on these agonistically as NE
drugs that selectively bind alpha-2 and act antigonistically as NE. This will prevent the inhibiting effect of alpha-2. More NE released into synaptic cleft and activation of postsynaptic receptors will be increased.
small;">Drugs that block the active re-uptake of NE back into the pre-synaptic neuronal terminal. By preventing the reuptake of NE back into the pre-synaptic cell, this decreases the NE in the presynaptic cell. This also cause a negative feedback loop for tyrosine hydroxylase enzame, creating more I-Dopa and essentially more NE. Overall there will be more NE acting on receptors
drugs that block the monoamineoxidase enzyme referred to as MAOIs, allow the concentration of NE in the pre-synaptic neuronal terminal to ↑. This in turn ↑s the amount of NE in synaptic vesicles, leading to ↑'d release of NE into synaptic cleft
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