Term
Amphetamine
tyramine
ephedrine
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Definition
| 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. |
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Term
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Definition
| drugs that mimic the action of NE at all adrenergic receptors in a non-selective manner |
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Term
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Definition
| drugs that only bind to the alpha-1 NE receptors on target organs and act agonistically to NE |
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Term
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Definition
| drugs that selectively bind to beta NE receptors and act agonistically to NE |
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Term
phenoxybenzmine
phentolamine |
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Definition
| 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 |
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Term
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Definition
| drugs that selectively bind to beta-1 NE receptors on target organ cells and act agonistically as NE |
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Term
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Definition
| drugs that selectively bind to beta-2 NE receptors on target organ cells and act on these agonistically as NE |
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Term
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Definition
| 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. |
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Term
cocaine
tricyclic antidepressants |
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Definition
| 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 |
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Term
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Definition
| 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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Term
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Definition
| selective alpha-2 agonists ↓ amount of NE released from presynaptic neuron and less neurotransmitter will reach post-synaptic target cells |
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Term
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Definition
| alpha-1 selective receptor blockers will inhibit action of NE only at target organs of the sympathetic nervous system with alpha-1 |
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Term
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Definition
| non-selective beta adrenergic receptor blockers will inhibit action of NE at target organs of sympathetic nervous system with both beta1&2 receptors |
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Term
betaxolol
atenolol
metoprolol |
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Definition
| selective beta-1 blockers |
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Term
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Definition
| drugs that compete with the active uptake of tyrosine. As a result when AP initiates release of neurotransmitter, there is much less NE released. a-methyl-NE does not activate post synaptic adrenergic receptors. |
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Term
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Definition
| Drugs that reverse the equilibrium of NE in the ICF and in the vesicles. As a result, little NE is inside the synaptic vesicles and a very large amount of NE in the ICF. Less NE released. |
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Term
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Definition
| Drugs that create a steady release of ACh from presynaptic neurons, bypassing normal processes |
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Term
bethanechol
methancholine |
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Definition
| drugs that act like ACh on muscarinic receptors agonistically |
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Term
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Definition
| drugs that act like ACh on nicotinic receptors agonistically |
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Term
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Definition
| drugs that inhibit the AChE enzyme |
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Term
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Definition
drugs that block the loading of ACh into the presynaptic vesicles
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Term
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Definition
| drugs that block the uptake of choline into the presynaptic cell |
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Term
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Definition
| drugs that block the fusion of presynaptic vesicles with the cell membrane. No ACh is released following AP |
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Term
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Definition
| drugs that directly block the nicotinic ACh receptor at postsynaptic ganglion. Drugs that block these recpetors reduce both sympathetic and parasympathetic impulses to the target organs. |
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Term
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Definition
| drugs that block nicotinic ACh receptors at voluntary muscles, these muscle cells do not depolarize to generate muscle contraction. This produces muscle relaxation |
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Term
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Definition
| drugs that bind agonistically to the nicotinic ACh receptors and remain bound for times much longer than just required to excite the muscle cells to contract. This will keep the postsynaptic muscle cells depolarized to a point beyond initial contraction. After a few seconds, the muscle cells will be unable to maintain contraction, and the muscle will finally completely relax. This causes muscle relaxation. |
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Term
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Definition
| Drugs that antagonistically block the muscarinic receptors, the response of the postsynaptic transmission is diminished. |
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