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Questions and Answers
What is the primary mechanism by which norepinephrine (NE) is removed from the synaptic cleft?
What is the primary mechanism by which norepinephrine (NE) is removed from the synaptic cleft?
- Uptake by the postsynaptic neuron
- Degradation by catechol-O-methyltransferase (COMT)
- Metabolism by monoamine oxidase (MAO)
- Uptake by the presynaptic neuron through a carrier protein (correct)
What is the result of the uptake 2 process in the removal of norepinephrine (NE)?
What is the result of the uptake 2 process in the removal of norepinephrine (NE)?
- NE is stored in the presynaptic neuron
- NE is removed from the synaptic cleft and degraded by COMT
- NE is taken up by the postsynaptic neuron (correct)
- NE is metabolized by MAO
What is the function of catechol-O-methyltransferase (COMT) in the metabolism of norepinephrine (NE)?
What is the function of catechol-O-methyltransferase (COMT) in the metabolism of norepinephrine (NE)?
- It breaks down NE into amino acids
- It methylates NE to form 3-methoxy-4-hydroxymandelic acid (correct)
- It oxidizes NE to form an aldehyde
- It converts NE to an inactive metabolite
What is the classification of adrenergic receptors that respond more strongly to norepinephrine (NE) than to isoproterenol?
What is the classification of adrenergic receptors that respond more strongly to norepinephrine (NE) than to isoproterenol?
What is the secondary messenger involved in the signaling pathway of adrenergic receptors?
What is the secondary messenger involved in the signaling pathway of adrenergic receptors?
What is the characteristic of alpha-adrenergic receptor agonists?
What is the characteristic of alpha-adrenergic receptor agonists?
What is the result of the metabolism of norepinephrine (NE) by monoamine oxidase (MAO)?
What is the result of the metabolism of norepinephrine (NE) by monoamine oxidase (MAO)?
What is the mechanism by which norepinephrine (NE) is reabsorbed into neurons?
What is the mechanism by which norepinephrine (NE) is reabsorbed into neurons?
What is the effect of stimulating α1 receptors in blood vessels?
What is the effect of stimulating α1 receptors in blood vessels?
Which neurotransmitter is NOT a member of the catecholamine family?
Which neurotransmitter is NOT a member of the catecholamine family?
What is the function of β2 receptors in the cardiac muscles?
What is the function of β2 receptors in the cardiac muscles?
What is the effect of NE administration on the uterus?
What is the effect of NE administration on the uterus?
What is the primary function of α2 receptors?
What is the primary function of α2 receptors?
Which of the following is NOT a physiological function regulated by adrenergic neurotransmitters?
Which of the following is NOT a physiological function regulated by adrenergic neurotransmitters?
What is the effect of adrenergic drugs on carbohydrate metabolism?
What is the effect of adrenergic drugs on carbohydrate metabolism?
What is the primary function of β2 receptors in skeletal muscles?
What is the primary function of β2 receptors in skeletal muscles?
What is the essential feature of direct acting sympathomimetics?
What is the essential feature of direct acting sympathomimetics?
What is the effect of replacing H with an alkyl group in direct acting sympathomimetics?
What is the effect of replacing H with an alkyl group in direct acting sympathomimetics?
Why do direct acting sympathomimetics exhibit stereoselectivity?
Why do direct acting sympathomimetics exhibit stereoselectivity?
Which of the following is NOT inactivated orally?
Which of the following is NOT inactivated orally?
What is the effect of β-OH group on receptor binding?
What is the effect of β-OH group on receptor binding?
What is the characteristic of R(-) enantiomer of direct acting sympathomimetics?
What is the characteristic of R(-) enantiomer of direct acting sympathomimetics?
What is the consequence of metabolic inactivation of direct acting sympathomimetics?
What is the consequence of metabolic inactivation of direct acting sympathomimetics?
What is the pharmacological effect of direct acting sympathomimetics?
What is the pharmacological effect of direct acting sympathomimetics?
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Study Notes
Termination of Action
- Norepinephrine (NE) may be removed from the action site through two processes: uptake and metabolism
- Uptake process: the greatest amount of NE is rapidly reabsorbed into neurons and then into its storage sites through an active transport mechanism (carrier protein)
- Two types of uptake: uptake 1 (highly stereospecific, occurs at nerve terminal on presynaptic cell membrane) and uptake 2 (less stereospecific, occurs at the receptor site on the postsynaptic cell membrane)
Metabolism
- NE is metabolized to inactive metabolites excreted in the urine
- Two enzymes involved in metabolism: Monoamine Oxidase (MAO) and Catechol-O-Methyltransferase (COMT)
- MAO converts NE into an acid or aldehyde
- COMT converts NE into 3-methoxy-4-hydroxymandelic acid
Adrenergic Receptors
- Adrenoreceptors are G protein-coupled receptors that are targets of catecholamines (NE and E)
- Classified into two types: α and β receptors
- α-adrenergic receptor primary binding involves a small N-substituent and at least one OH
- β-adrenergic receptor primary binding involves a bulky N-substituent and two catecholic OHs
- α1 or α2 response is stronger to NE or E than isoproterenol
- β1, β2, or β3 response is stronger to isoproterenol than E or NE
Sympathomimetic Drugs
- Direct-acting sympathomimetics are phenylethylamine derivatives
- Structure-activity relationship (SAR) requirements:
- β-OH is essential
- N atom should bear at least one H (1ry or 2ry)
- N atom should be separated from the ring by 2 C
- 3-OH and 4-OH are important for activity
- Vasoconstrictor activity is increased by replacing H with alkyl groups (increases lipophilicity)
Adrenergic Drugs
- Adrenergic drugs stimulate or inhibit adrenergic receptors (α and β receptors)
- Adrenergic neurotransmitters regulate many physiological functions, including:
- Blood pressure
- Heart rate
- GIT motility
- Bronchial tone
- Carbohydrate metabolism
- Transport of lipid from fat depots to the liver
- NE is a neurotransmitter in the autonomic nervous system and in the CNS
Adrenergic Receptors and Physiological Functions
- α1 receptors: stimulation causes vasoconstriction
- α2 receptors: mostly postsynaptic
- β2 receptors: stimulation causes:
- Increased heart rate and various arrhythmias
- Contraction of skeletal muscles
- Increased GIT motility and pancreatic secretion
Catecholamines
- Include NE, E, and dopamine
- Chemical structures:
- NE: OH, NH2, HO
- E: OH, N, HO, NH2
- Dopamine: OH, NH2, HO
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