Parasympathetic System and Neurotransmitter Biosynthesis/Metabolism - VOCAB Flashcards

Vocabulary flashcards covering parasympathetic system, acetylcholine metabolism, and adrenergic biosynthesis/metabolism as described in the notes.

Parasympathetic system

Aka cholinergic system; autonomic division using acetylcholine as the primary neurotransmitter; receptors are muscarinic (G protein–coupled) and nicotinic (ligand-gated ion channels); located at the neuromuscular junction and autonomic ganglia; acetylcholinesterase (AChE) metabolizes ACh to choline and acetic acid.

Acetylcholine (ACh)

Primary neurotransmitter of the parasympathetic system; rapidly hydrolyzed by AChE into choline and acetic acid; acts at muscarinic and nicotinic receptors.

Muscarinic receptor

G protein–coupled receptor for ACh; mediates parasympathetic postganglionic responses.

Nicotinic receptor

Ligand-gated ion channel receptor for ACh; located at the neuromuscular junction and autonomic ganglia.

Acetylcholinesterase (AChE)

Enzyme that hydrolyzes acetylcholine to choline and acetic acid.

Choline acetyltransferase (ChAT)

Enzyme that synthesizes ACh from choline and acetyl-CoA.

Serine decarboxylase

Enzyme that converts L-serine to ethanolamine (part of acetylcholine biosynthesis).

Choline-N-methyl transferase

Enzyme converting ethanolamine to choline (as described in the notes).

Ethanolamine

Intermediate in acetylcholine biosynthesis formed from serine decarboxylation; precursor to choline.

Bethanechol

Cholinergic agonist used to stimulate GI tract and urinary bladder after surgery; relatively resistant to hydrolysis, providing longer action.

Carbachol

Cholinergic agonist with a carbamate group; less prone to hydrolysis and longer-acting; used for glaucoma.

Methacholine

Cholinergic agonist with an added alkyl group; more selective for muscarinic receptors; used for diagnosis of asthma.

AChE metabolism products

Acetylcholine is hydrolyzed by AChE to choline and acetic acid.

Norepinephrine (NE)

Catecholamine involved in BP regulation in the peripheral nervous system; produced from dopamine via dopamine β-hydroxylase; metabolized by MAO and COMT to vanillylmandelic acid (VMA).

Epinephrine (E)

Potent bronchodilator and vasoconstrictor; produced from norepinephrine via PNMT; used in anaphylactic shock and other urgent settings.

Dopamine

Catecholamine formed from L-DOPA via aromatic L-amino acid decarboxylase; precursor to norepinephrine; metabolized to HVA via MAO and COMT.

Phenylethanolamine N-methyl transferase (PNMT)

Enzyme converting norepinephrine to epinephrine (primarily in the adrenal medulla).

MAO (Monoamine oxidase)

Enzyme that degrades monoamines including catecholamines (NE, E, dopamine) to aldehydes and acids.

COMT (Catechol-O-methyl transferase)

Enzyme that methylates catecholamines, contributing to their inactivation (to VMA or similar).

VMA (Vanillylmandelic acid)

End product of catecholamine metabolism (NE and E); used as a clinical marker for catecholamine levels (e.g., pheochromocytoma).

HVA (Homovanillic acid)

End product of dopamine metabolism; used as a marker in neurological disorders such as Parkinson’s disease.

Dobutamine

β1-adrenergic receptor agonist; increases cardiac output; used in cardiogenic shock.

Septic shock treatment context

Norepinephrine is commonly used as a vasopressor to raise blood pressure.

Anaphylactic shock treatment context

Epinephrine is the drug of choice; bronchodilation and vasoconstriction counteract severe allergic reactions.

Cardiogenic shock treatment context

Dobutamine used to stimulate β1-adrenergic receptors and increase cardiac output.

β-Phenyl ethylamine (parent SAR structure)

Parent structure in structure-activity relationship (SAR) of adrenergic agonists; two carbon atoms separate the ring from the amino group.

Optical isomerism (1R configuration)

1R configuration associated with more potent adrenergic activity.

Substitution on nitrogen (N)

Larger/bulkier N-substituents increase β-agonist activity and reduce α-agonist activity, aiding development of β-selective agonists.

Substitution on the α-carbon

Blocking MAO oxidation increases duration of action; increases oral absorption and CNS activity; methylation can shift selectivity toward α2 receptors.

3’ and 4’ hydroxyl groups on the aromatic ring

Presence yields maximal α and β activity and supports direct-acting activity; absence can confer indirect activity and resistance to COMT; 3’ OH favors α-activity, 4’ OH favors β-activity.