Drugs affecting Cholinergic and Adrenergic receptors
Rule of Thumb on Oxidation
In general, in aromatic rings:
The position that is electron-rich
Has the least steric hindrance
This position gets oxidized to form the metabolite.
Structure of the Peripheral Nervous System
The nervous system is divided into PNS and CNS. The PNS serves as a communication network that links the CNS to the rest of the body
Divisions:
Autonomic: Responsible for regulating involuntary bodily functions.
Somatic: Controls voluntary movements and is responsible for transmitting sensory information to the CNS and sending motor signals from the CNS to receptors in the skeletal muscles through motor nerves.
Autonomic Nervous system:
ANS is futher divided into Sympathetic and Parasympathetic Nervous system
Sympathetic Nervous System: Prepares the body for 'fight or flight' responses, increasing heart rate, dilating pupils, and inhibiting digestion.
Parasympathetic Nervous System: Promotes 'rest and digest' activities, slowing the heart rate, constricting pupils, and stimulating digestive processes.
Neurotransmitters:
The sympathetic and parasympathetic have receptors in smoth and cardiac muscle.
ACh (Acetylcholine) neurotransmitter used to transmit signals in both the sympathetic and parasympathetic nervous systems, playing a crucial role in muscle activation and various autonomic functions.
NA (Noradrenaline) used to transmit signals primarily in the sympathetic nervous system, influencing the body's 'fight or flight' responses.
Cholinergic Signaling System
Main Effects of Parasympathetic Transmission:
Increased tear secretion
Eye pupil contraction
Increased salivation
Decreased heart rate
Bronchial contraction
Increased gastrointestinal activity
Transmitter Used: Acetylcholine
Cholinergic Receptors
Types of Cholinergic Receptors:
Acetylcholine
Nicotine
L-(+)-Muscarine
Muscarinic Receptors & Acetylcholine
Receptor Types:
M1R, M2R, M3R, M4R, M5R
Function of Acetylcholine:
Acts via different muscarinic receptors for varied physiological effects (e.g., neuromodulation)
Muscarinic Receptor Binding Site
Key Features:
Hydrophobic pockets involved in binding
Specific amino acids and their arrangements are crucial for receptor interaction
Biosynthesis of Acetylcholine
Components:
Serine
Choline
Enzymatic Steps:
Decarboxylase produces Serine-derived substrates.
Acetylation of Choline by Choline Acetyltransferase
Cholinergic Synapse
Structure of Synapse:
Presynaptic and postsynaptic cells connected via neurotransmitter release
Key Steps:
Acetylcholine and choline synthesis
Release and recycling across the synapse
Cholinergic Drugs
Types of Cholinergic Drugs:
Direct acting: Activate receptors directly
Indirect acting: Prevent degradation of acetylcholine, increasing receptor activation.
Direct Acting Cholinergics
Applications:
Treatment of glaucoma (lowers intraocular pressure)
Examples:
Pilocarpine
Carbachol
Acetylcholine eye drops
All examples have similar pharmacophore: an ester, alkyl linker and positivly charged amine.
Muscarinic Receptor Binding Sites
Key Residues:
Trp-307, Asp-311, Trp-613, Trp-616, Asn-617, etc.
Significance:
Influence on receptor activation by ligands.
Structure-Activity Relationships (SAR) for Cholinergics
Factors Affecting Activity:
Correct distance between nitrogen and oxygen in structure
Placement of small alkyl groups close to functional groups
Indirect Acting Cholinergics
Function:
Inhibit acetylcholinesterase enzyme, preventing acetylcholine degradation.
Uses:
Myasthenia gravis
Alzheimer's Disease
Acetylcholinesterase Structural Features
Key Amino Acids Involved:
Histidine, Serine, Glutamic acid
Mechanism of Action:
Interaction with acetylcholine and subsequent hydrolysis.
Acetylcholinesterase Mechanism
Role of Catalysts:
Serine acts as a nucleophile attacking the carbonyl carbon of the acetylcholine, facilitating the cleavage of the ester bond and leading to the formation of choline and acetate.
Histidine acts as both base and acid in this catalytic triad mechanism.
Anticholinesterases - Mechanism and Application
Anticholinesterases inhibit the activity of acetylcholinesterase.
Natural Products:
Neostigmine, Pyridostigmine
Mechanism:
Carbamoyl group transfer to Ser200 in active sites
Anticholinesterases Structural Characteristics
Serine residue in anticholinesterases acts as a nucleophile and attacks physostigmine while a histidine residue acts as both base and acid in this catalysis.
A stable carbamoyl intermediate will form leading to slow hydrolysis.
Anticholinesterases in CNS
Importance:
Attain efficacy in diseases like Alzheimer's Disease
Example: Rivastigmine.
Irreversible Acetylcholinesterase Inhibitors
Examples:
Organophosphorus compounds (e.g., Sarin, Tabun)
Mechanism:
Bind irreversibly to active site serine residues of acetylcholinesterase, preventing degradation of acetylcholine.
Antidotes to Organophosphate Poisoning
Example: Pralidoxime (Pro-2-PAM iodide)
Action:
Reverses the phosphorylation of serine residues in acetylcholinesterase.
Anticholinergic Drugs
Function:
Block acetylcholine action at muscarinic receptors (G-protein-coupled receptors)
Effects:
Eye pupil dilation, decreased salivation, decreased GI secretion.
Natural Products as Anticholinergics
Major natural sources:
Hyoscyamus niger, Atropa belladonna, Datura stramonium
Semisynthetic Anticholinergics
Compounds like Methylscopolamine and Ipratropium for specific therapeutic actions.
Synthetic Anticholinergics
All have an aromatc ring connected with a ring and an ester linkage leadning to an ionised amine.
Function:
Provide spasmolytic effects.
Synthetic Anticholinergics for Urologic Use
Examples like Emepron and Tolterodine
Use:
Treat urologic spasm.
CNS Targeting Synthetic Anticholinergics
Used for treating Parkinson's disease
Compounds must pass blood-brain barrier.
Synthesis of Acetylcholinesterase Inhibitors
Learn the different synthetic tools used for organic synthesis
Synthesis of Anticholinergics
Learn the different synthetic tools used for organic synthesis
The Adrenergic Nervous System
Also known as the sympathetic nervous system
Uses a variety of neurotransmitters, including norepinephrine and epinephrine, to mediate the body's fight or flight response.
Results:
Sympathetic effects like increased heart rate and relaxation of smooth muscles.
Page 35: Adrenergic Receptors
Types:
Alpha and Beta receptors
General:
Agonism at alpha-receptors → contraction noradrenaline > adrenaline > isoprenaline
Agonism at beta-receptors → relaxation
isoprenaline >> adrenaline > noradrenaline
Response Type:
Varies with agonism and hormone interaction (e.g., norepinephrine and adrenaline).
Alpha Receptors
Types: Alpha1 and Alpha2
Function:
Alpha1: Smooth muscles contraction, such as in blood vessels and pupils.
Alpha2: Inhibition of neurotransmitter release, leading to decreased sympathetic outflow and reduced blood pressure.
Mechanism of Alpha Receptors
Alpha1 Mechanism:
Gq pathway causing calcium release - contributing to muscle contraction.
Causes pupillary dialation, vasoconstriction etc.
Beta Receptors and Mechanisms
Receptor Types:
Beta1, Beta2, and Beta3
Increases cAMP
General Function:
Beta 1: Inceases heart rate and renin release in kidneys
Beta 2: Enhance airflow in lungs and smooth muscle relaxation
Beta 3: Stimulates breakdown of fat in dipose tissue
Biosynthesis of Noradrenaline
Learn the different synthetic tools used for organic synthesis
Process:
Tyrosine → Levodopa → Dopamine → Noradrenaline.
Synthesis, release and regulation of Norepinephrine
Tyrosine is the precursor for NE synthesis, which is first converted to DOPA and then dopamine in the nerve terminal. Dopamine is then converted to NE in synaptic vesicles.
NE is released upon nerve stimulation in the synaptic cleft (space between the nerve terminal and the target cell) and binds to receptors on the target cell to exert its effects.
NE action is regulated by reuptake mechanisms and feedback inhibition.
Certain drugs, like cocaine, interfere with NE reuptake, enhancing its action.This leads to increased levels of NE in the synaptic cleft, resulting in heightened physiological responses such as elevated heart rate and increased blood pressure.
Inactivation of Norepinephrine
By inhibiting the reuptake of NE to the nerve terminal, the action of NE is inactivated.
Methabolic pathways involving COMT and MAO-A.
Adrenergics - Sympatomimetics
Direct acting adrenergic agonists bind directly to adrenergic receptors, mimicking the effects of neurotransmitters like norepinephrine and epinephrine.
Indirect acting adrenergic agonists, on the other hand, enhance the release of norepinephrine from nerve terminals or inhibit its reuptake, thereby increasing its availability at the receptor sites.
Alpha-Receptor Agonists Structure
Alpha-agonists: (R)-noradrenaline, (R)-adrealine, dipivephrine.
Usually two hydroxyl groups ortho to each other on aromatic ring
Alpha1-aginists: (R)-phenylephrine, (R)-norphenephrine
Usually one hydroxyl group on aromatic ring
Beta-Receptor Agonists Structure
Unselective beta1/beta2-agonists: (R)-adrenaline, isoprenaline, orciprenaline
Usually two hydroxyl groups ortho to each other on aromatic ring
Selective beta1-agonists: erilephrine
Usually one hydroxyl group on aromatic ring
Synthetic Beta2-Receptor Agonists
Examples like Salbutamol and Formoterol for treating asthma.
Structure-Activity Relationships (SAR) of Adrenergics
The presence of a bulky side chain enhances selectivity for beta-receptors, while small side chain enhances selectivity for alfa-receptors.
Only primary or secondary amine
R-enatiomer most active
Removal of OH group ortho to the other OH group on aromatic ring enhances selectivity for alpha1/beta1 receptors
Presence of OH group meta to the other OH group enhances selectivity towards beta 2 receptors
Stabilization of Catecholamines
Catecholamines are important neurotransmitters that play a crucial role in the body's response to stress, regulating heart rate, blood pressure, and glucose metabolism.
Examples dopamine, norepinephrine and epinephrie
Catecholamines are easily oxidized
Prevent oxidation by addition of sodium pyrosulphite or EDTA
Antiadrenergics Overview
First generation beta-receptor blockers.
partially agonists
Unselective beta1/beta3-receptor blockers
Second generation beta-receptor blockers.
good antagonists
Unselective beta1/beta3-receptor blockers
Third generation beta-receptor blockers.
Provides selective blockade of beta-1 receptors, minimizing side effects on beta-2 receptors and enhancing therapeutic efficacy.
SAR antiadrenergics
S-enatiomer most active
Only secondary amines
Bulky side chains
Aromatic system is necessery
Ether directly linked to the aromatic system is often present but not necessary
Synthesis of Antiadrenergics
Learn the different synthetic tools used for organic synthesis
Synthesis of beta-receptor blockers
Learn the different synthetic tools used for organic synthesis
Key Topics to Remember
The structures of acetylcholine, noradrenaline and adrenaline
The difference between direct and indirect acting cholinergics
SAR cholinergics
SAR acetylcholinesterase inhibitors
Irreversibel inhibitors of acetylcholinesterase - pralidoxime antidote
SAR anticholinergics
Synthesis of drugs acting at cholinergic receptors or at acetylcholinesterase
The difference between direct and indirect acting adrenergics
SAR adrenergics (alpha-receptor selective vs beta-receptor selective)
SAR antiadrenergics
Synthesis of drugs acting at adrenergic receptors.