PHARMACOLOGY

CHOLINERGIC AGONIST increase in calcium and increase in

contraction
Cholinergic agonist When IP3 is inhibits there would be
- Its effect is bronchoconstriction decrease in calcium and decrease in
contraction
Cholinergic antagonist
IP3 inhibits PDE (phosphodiesterase
- Its effect is bronchodilation enzyme)
Nicotinic antagonist PDE
 Neuromuscular junction blockers  Responsible for the metabolism of
 Also block the nicotinic neural which is cAMP  cause contraction in the
the ganglion blockers heart/ decrease in contraction
 When PDE is inhibited there would be
Cholinoceptor antagonist
increase in cAMP thereby producing too
 Red as a beet much contraction that will cause
 Cause flushing of skin TACHYCARDIA
 Hot as hell
 hyperthermia b) Scopolamine
 Dry as a bone  Can be used as one of the ingredients of
 decrease in secretion truth serum  is a component of
 Blind as bat twilight sleep which is composed of
 cycloplegia, blurring of vision, glaucoma morphine + scopolamine
 Mad as hatter Truth serum
 delirum  Physicians noted that women in twilight
Muscarinic antagonist sleep answered questions accurately

 inverse agonist  opposite of the effect c) Homatropine

of cholinergic agonist
 Muscarinic blockers
 Used to block the M1, M2 and M3
receptor
a) Atropine
 It is a racemic mixture
 Prototype drug of muscarinic blockers
 Peristalsis of the gastro intestinal tract
 Atropine + Diphenoxylate = Lomotil
Local source: Datura metel  talumpunay
Ophthalmoscopic examination
 Used for diagnostic test of
ophthalmologic disorder along with
cyclopentolate and tropicamide
d) Ipratropium
 Used as an anti-asthma drugs
 Ipratropium + Albuterol = Combivent
e) Pirenzepine
 It is an anti-ulcer drug

Common side effects: Tachycardia f) Benztropine

 Used in Parkinson’s disease
MOA: IP3 is a secondary messenger, when
there is an increase in IP3 there would be
 PHARMACOLOGY

Synechiae Neuromuscular blockers/ Skeletal muscle

 A condition where in the iris adheres to receptor
the cornea or the lens
 Causes paralysis
Treatment: homatropine
 Two types: depolarizing blocker and
non- depolarizing blocker
Uveitis
 Inflammation of the middle layer of the Non- Depolarizing blocker Depolarizing blocker
eye Antagonist of ACH Agonist of ACH
Iritis Competitive Non-competitive
 Inflammation of the iris
Cause depolarization 
No ACH effects would fasciculation (spastic
Respiratory disorder cause relaxation of muscle paralysis)  desenzitation
that leads to flaccid of receptor  repolarization
 Tiotropium
paralysis  relaxation  flaccid
BN: Spiriva
paralysis
 Tiotropium + Formoterol
 Tiotropium + Fluticasone + Salmetarol Example: Example:
Urinary disorder Tubocurarine Succinylcholine
Produce a skeletal muscle
 Oxybutynin relaxation
 Meningomyelocele  also called the
spina bifida  (side effect of
lamotrigine and valproic acid) which is a
birth defect where there is incomplete
closing of the backbone and
membranes around the spinal cord

Cholinergic drugs that causes toxicity/

poisoning:

 Organo phosphate

NICOTINIC BLOCKING AGENTS

Ganglionic blockers  inhibits the nicotinic

neural

1. Tetraethylammonium
2. Hexamethonium
 1st effective antihypertensive drug
3. Decamethonium
 PHARMACOLOGY
CHOLINOCEPTOR ANTAGONISTS Uveitis
- Inflammation of the middle layer of the
Ganglion blockers eye

- Block/inhibit nicotinic neural receptors Iritis

Effects of Cholinoceptor Antagonists - Inflammation of iris

 Flushing of skin
 Hyperthermia (increased temp.) TIOTROPIUM
 Decrease in secretion
- Brand name is SPIRIVA
 Cycloplegia, blurring of vision and
- Combined with FORMOTEROL
glaucoma
 Delirium - Tiotropium + Fluticasone + Salmeterol
- Anti-asthma
MUSCARINIC BLOCKERS
OXYBUTYNIN
A. ATROPINE
- Prototype muscarinic blocker - Bladder is relaxed, sphincter is closed
- Racemic (can be + or -) leading to urinary retention
- Can also be gained from Datura metel - Used in MENINOMYELOCELE or SPINA
or talumpunay (local source in BIFIDA – a birth defect where there is
Philippines) an incomplete closing of the backbone
- Leads to the low amounts of IP3  and the membranes around the spinal
decrease calcium  DECREASED in cord (S/E off LAMOTRIGINE or
MUSCLE CONTRACTION VALPROIC ACID)
- Inhibits PDE (phosphodiesterase
enzyme) for the metabolism of CAMP BOTULINUM toxin
leading to HEART CONTRACTION 
TACHYCARDIA (common side effect) - Blocks ACH or acetylcholine
- Formerly Atropine + Diphenoxylate = ORGANOPHOSPHATES
LOMOTIL (anti-peristalsis)
B. SCOPOLAMINE - Usually causes cholinergic poisoning
- Ingredient in TRUTH serum, a
component of Twilight Sleep, together
with morphine
NICOTINIC BLOCKER
C. HOMATROPINE
D. IPRATROPIUM 1. Ganglionic blockers
- Ipratropoum + Albuterol = COMBIVENT - Can inhibit sympathetic or
E. PIRENZEPINE parasympathetic ganglion
- Anti-ulcer A. Hexamethonium
F. BENZOTROPINE - The first effective antihypertensive drug
- Anti-Parkinson’s diseases
under ganglionic blockers

Synechiae
- Condition where the iris adheres to the
cornea or the lens
 PHARMACOLOGY
2. NEUROMUSCULAR BLOCKERS

Non-depolarizing Depolarizing blocker

blocker
Antagonist of ACH Agonist of ACH
Competitive Non-competitive
No ACH effects or Depolarization (Phase 1)
RELAXATION  (FASCICULATION/SPASTIC
FLACCID PARALYSIS PARALYSIS) leading to
DESENZITATION (Phase 2)
 REPOLARIZATION 
No impulse 
RELAXATION (FLACCID
PARALYSIS)
Prototype is Most common drug is
TUBOCURARINE SUCCINYLCHOLINE
Produces SKELETAL Produces SKELETAL
MUSCLE MUSCLE RELAXATION
RELAXATION
CLOSES channel OPENS and BLOCKS
channel

SUMMARY

MUSCARINIC BLOCKERS

- Prototype is ATROPINE

NICOTINIC BLOCKERS

A. Ganglion blocker  blocks Nn

- Prototype drug is HEXAMETHONIUM
B. Neuromuscular blocker  blocks Nm
B.1. Non-depolarizing
- prototype is TUBOCURARINE
B.2. Depolarizing
- prototype is SUCCINYLCHOLINE