Types of receptors

Class Structure Important locations Effect of stimulation

Metabotropic Adrenergic Alpha-adrenergic Alpha-1 Gq proteins 1.Smooth muscle: 1.Peripheral

receptors: receptors receptors receptor -Blood vessels vasoconstriction
G-protein-coupled -Bladder trigone, Arterioles →↑ afterload
receptors acting sphincter and Veins →↑ preload
through second prostatic urethra 2.Bladder sphincter
messengers (see -Eye (iris dilator contraction → urinary
signal transduction) muscle) retention
-GI tract 3.Mydriasis
4.GI sphincter
contraction (no
defecation)

Alpha-2 Gi proteins 1.Prejunctional nerve 1. Inhibition of

receptor terminals transmitter release
2.Pancreas ↓ Norepinephrine
release and synthesis
(negative feedback)
2. Inhibition of insulin
release
↓ Insulin release

Beta-adrenergic Beta-1 Gs proteins 1.Heart 1.Cardiac excitation

receptors receptor -SA node ↑ Heart rate
-AV node (chronotropy)
-Atrial and ↑ Conduction velocity
ventricular muscle (dromotropy)
2.Kidney ↑ Force of contraction
(inotropy)
2. Renin secretion
↑ Renin release

Beta-2 Gs proteins 1.Smooth muscle 1.Relaxation of smooth

receptor -Blood vessels muscle
-Bronchioles Vasodilation
-Uterus Bronchodilation
2.Skeletal muscle Relaxation of uterus
3.Liver Bladder relaxation
4.Pancreas 2.Increases contractility
↑ Contractility (tremors)
3. ↑ Glycogenolysis
(increases hepatic output
of glucose)
4. ↑ Glucagon release

Beta-3 Gs proteins 1.Adipose tissue 1.↑ Lipolysis

receptor
 Cholinergi Muscarinic M1 Gq protiens 1. Gastric parietal 1.Increased gastric
c receptors acetylcholine cells secretion and motility
receptors
M2 Gi proteins 1. Myocardium 1.Myocardial inhibition
2. Presynaptic nerve 2.Inhibition of
terminals neurotransmitter release
3.Sphincters 3.Sphincter relaxation

M3 Gq proteins 1.Smooth muscles of 1. ↑ Secretion of

glands exocrine glands (e.g.,
-Salivary lacrimation, salivation,
-Lacrimal hidrosis)
-Sweat 2.Contraction of the
2.Eye following muscles in the
3.Bronchi eye
4.Bladder Iris sphincter muscle →
miosis
Ciliary muscle →
accommodation
3.Bronchospasm
4.↑ Urination
Contraction of detrusor
Relaxation of sphincter

M4 Gi proteins 1.CNS Inhibitory

(M4)/excitatory (M5)
M5 Gq proteins 1.CNS Memory
Arousal
Attention
Analgesia

Ionotropic receptors Nicotinic Nm Ligand-gated 1.Neuromuscular 1.Skeletal muscle

acetylcholine ion channel junction of skeletal contraction
receptors muscle (somatic
nervous system)

Nn 1.Autonomic ganglia 1.Facilitate

neurotransmission
Sympathomimetics Drug Mechanism of action Clinical use

Directly acting Non Adrenaline Non selective agonist 1.Cardiac arrest

selective a1 = a2 = b1= b2 2.Anaphylactic shock
(anaphylaxis is the most severe
form of an allergic reaction and is
life threatening)
3.Status asthmaticus (an
extreme form of asthma
exacerbation characterized by
hypoxemia, hypercarbia, and
secondary respiratory failure)
4.Prolongation of local
anesthetic effect

Noradrenaline Non selective agonist 1.Hypotension

a1> a2=b1 2.Septic shock (a
life-threatening condition that
happens when your blood
pressure drops to a dangerously
low level after an infection)

Dopamine d1=d2 >b1> a1 1. Cardiogenic shock (heart

suddenly can't pump enough
blood to meet your body's needs,
the condition is most often caused
by a severe heart attack)
2.Congestive heart failure (a
long-term condition in which
your heart can't pump blood well
enough to meet your body's
needs)

Isoproterenol b1=b2 1.Bradycardia

(synthetic) 2.AV blockade

Selective Phenylephrine a1 selective agonist 1.Nasal decongestant

2.Hypotension

Clonidine Centrally acting a2 1.Hypertension

selective agonist

Dobutamine b1 selective agonist 1.Cardiogenic shock

2.Congestive heart failure

Salbutamol b2 selective agonist 1.Bronchial asthma

Indirectly acting Releasing Amphetamine Increases 1.Attention
agent noradrenaline release deficit/Hyperactivity disorder
+ non selective 2.Used as an appetite
agonist a1=a2=b1=b2 suppressant (obesity)

Uptake Amitriptyline Noradrenaline 1.Depression

inhibitor reuptake inhibitor

Cocaine Noradrenaline 1. Local anesthesia

reuptake inhibitor 2. Vasoconstriction

MAO/ Selegiline MAO inhibitor 1. Parkinson's disease

COMT
inhibitor

Mixed acting Non Ephedrine a1=a2=b1=b2 1.Asthma (no longer used)

selective + Increases 2.Nasal decongestant
indirect noradrenaline release
Alpha receptor antagonist (Sympatholytic)

Class Drugs MOA Indication (use of that Adverse effects

drug for treating a
particular disease)

Nonselective Blocks both Phentolamine 1. a1 receptor 1.Hypertensive 1.Reflex

alpha receptor a1 and a2 antagonist emergencies tachycardia
antagonists receptors causes -Tyramine ingestion in 2.Orthostatic
reversibly vasodilation in patients on MAO hypotension
both arterioles inhibitors 3.Nasal stuffiness
Blocks both Phenoxybenzamine and veins -Cocaine-induced 4.Failure of
a1 and a2 hypertension ejaculation
receptors 2. a2 receptor (second-line)
irreversibly antagonist (Control episodes of
potentiates the hypertension and other
release of adverse effects due to
epinephrine and excess catecholamine)
norepinephrine -Pheochromocytoma
from nerve (a catecholamine-secreting
endings thus, tumor that originates from
causing chromaffin cells in the
tachycardia adrenal medulla. Causes
sustained or paroxysmal
hypertension with episodic
blood pressure crises,
paroxysmal headaches,
diaphoresis, palpitations,
and pallor due to excess
epinephrine,
norepinephrine, and
dopamine secretion)

Alpha-1 receptor Potent and Prazosin,Doxazosin 1. a1 receptor 1.Systemic hypertension 1. First dose
antagonists selective a1 blockade in 2.Benign hyperplasia of hypotension
receptor arterioles and prostate (within 30-60
antagonist veins which mins of 1st dose)
causes 2.Syncope with
vasodilation and rapid increase in
reduced BP dose
3.Orthostatic
hypotension
4.Headache,
dizziness
5. Nasal stuffiness
Beta receptor antagonist (Sympatholytic)

Class Drugs MOA Indication (use of that Adverse effects

drug for treating a
particular disease)

Cardioselective beta blockers (β1 Metoprolol, 1.Without ISA 1.Hypertension 1.Bradycardia

selective Bisoprolol, 2.Less risk of 2.Cardiac arrhythmia 2.Bradyarrhythmia
Atenolol, bronchoconstriction 3.Coronary heart 3.Cardioselectivity is
Esmolol, 3,Less risk of disease dose-dependent: β2
Nebivolol metabolic 4.Compensated heart receptor blocking
abnormalities failure activity increases
4. Ineffective in 5.Angina with higher doses .
suppressing tremors 4.Generally do not
cause
bronchoconstriction
or vasoconstriction
5.Generally do not
interfere with
glycogenolysis; safe
in diabetic patients

Nonselective beta blockers (β1, Propranolol 1.Without ISA 1.Hypertension 1.Common:

β2, and β3receptors) 2.Prototype, non 2.Ischemic heart -dizziness,fatigue,de
selective competitive disease pression
antagonist at beta 3.Cardiac 2.Chronic use:
receptors arrhythmias -worsening
3.Mechanism: 4.Congestive cardiac metabolic profile
-blocks existing failure 3.In diabetics:
sympathetic tone 5.Hyperthyroidism -Pregnant
-decreases HR, CO (anxiety tremors) hyperglycaemic
and pacemaker 6.Migraine response
activity prophylaxis (adrenaline) during
-slow resistance in 7.Glaucoma hypoglycemia
peripheral resistance 8.Anxiety -masks signs of
4.Pharmacokinetics: 9.Essential tremors hypoglycemia that
-well absorbed are important to
following oral diabetic patients
administration 4.Sudden withdrawal
-high lipid syndrome:
solubility:can -rebound
penetrate BBB hypertension,
(drowsiness) anginal attack &
-extensive possibly MI if drug
(significant) first pass suddenly withdrawn
 metabolism after chronic therapy
5.Contraindications:
-Asthma and COPD
-Decompensated
heart failure
-Heart block
-Cardiogenic shock

Pindolol 1.With ISA 1.Exerts effects like

2.b1 and b2 partial epinephrine in high
agonist doses
3.More suitable for
patients prone to have
bradycardia/bronchial
asthma compared to
full antagonists
4.Less suitable for
patients with history
of ischemic heart
disease
5.Withdrawal less
likely to cause
rebound hypertension/
angina

Nonselective beta blockers (β1, Labetalol 1.Selective a1 blocker 1.Pregnancy induced 1.Contraindications:
β2, and β3receptors) with and non selective b1 hypertension -Asthma and COPD
additional α-blocking action and b2 blocker 2.Hypertensive -Decompensated
-complex action emergencies heart failure
causes decrease in (intravenous) -Heart block
systemic arterial BP -Cardiogenic shock
and vascular
resistance without a
reduction in HR, CO
or stroke volume
Cholinergic agonist (Parasympathomimetic drugs)

Class Drugs MOA Indication (use of that drug Adverse effects

for treating a particular
disease)

Directly acting Acetylcholine Muscarinic and 1.Not used clinically

nicotinic agonists 2.Very short duration of
action because it’s rapidly
hydrolysed by
acetylcholinesterase and
plasma cholinesterase

Pilocarpine Muscarinic 1.Treatment of glaucoma 1.Local irritation

-Open-angle and 2.Too toxic for
Can cross closed-angle glaucoma systemic use
blood-brain barrier ↑ Contraction of ciliary
(tertiary amine) muscle of the eye Contraindications:
↑ Contraction of pupillary 1.Asthma
sphincter 2.Peptic ulcer
2.Xerostomia (dryness of 3.Coronary
the mouth) vascular disease
Xerostomia (e.g., in
Sjogren syndrome): ↑
sweat, tears, and saliva
production

Pharmacological effects:
-miosis
-spasm of accommodation
-decrease intraocular
pressure

Methacholine 1. To diagnose bronchial 1.Bradycardia

hyperreactivity (bronchial Contraindications:
Can not cross challenge test) 1.Asthma
blood-brain barrier 2.Peptic ulcer
(quaternary amine) 3.Coronary
vascular disease

Bethanechol 1.Postoperative and

neurogenic ileus and
urinary retention:
↑ bladder smooth muscle
tone
 Nicotine Nicotinic

Suxamethonium MOA under NM blockers

chloride

Indirectly acting Edrophonium Reversible: Short acting 1.Increases acetylcholine

(cholinesterase concentration in
inhibitors) neuromuscular junctions
for short time (2 to 10
mins)

2.Used to diagnose
myasthenia gravis (tensilon
test)

Neostigmine Reversible:Medium 1.Forms a moderately

acting stable bond with AchE,
bond is hydrolysed much
more slowly compared to
Ach
2. Increases Ach levels at
NMJ
3.Increases strength of
muscle contraction in
patients with myasthenia
gravis for hours

2.Paralytic ileus (condition

where the motor activity of the
bowel is impaired, usually
without the presence of a
physical obstruction)
3.Atonic bladder (a condition
where the detrusor muscle in the
bladder loses its ability to
contract, making emptying the
bladder difficult)
4.To reverse the effects of
neuromuscular blockers

Physostigmine 1.Glaucoma
(tertiary amine hence 2.Treatment of atropine
it is lipid soluble and poisoning
can cross BBB which
can lead to CNS
toxicity)
Tacrine Reversible:Long acting 1. More lipophilic, thus has
a longer duration of action
2.Acts in CNS and used to
treat Alzheimers

1.Organophosphates Irreversible 1.Forms a strong covalent Antidote:

-isoflurophate bond with AchE -Pralidoxime
-echothiophate 2.Bond is hydrolysed (enzyme activator)
extremely slowly and -Atropine
2.Soman, Sarin undergoes ‘aging’ after (muscarinic
(nerve gas) some time where it no antagonist) in large
3.Malathion longer can be broken doses as often as
(insecticides) 3.Enzyme can be required
reactivated by
oximes(Pralidoxime) if
given before aging occurs
4.Irreversible inactivation
of AchE causes prolonged
increase in Ach levels,
resulting in toxic effects
Muscarinic antagonist

Class Drugs MOA Effect Indication (use of that drug

for treating a particular
disease)

Tertiary amines Atropine 1.Non specific 1.System effects: 1.First drug of choice in
Lipophilic antagonist - Increased ↑ Heart rate unstable (symptomatic)
(good oral (M1-M5) -Decreased ↓ Secretions of sinus bradycardia (IV)
bioavailability and 2.Reversible and exocrine glands (difficulty 2.Premedication: prior to
CNS penetration) has a long half life swallowing and speaking) intubation to decrease
-Decreased ↓ Tone and salivary, respiratory, and
motility of smooth muscles gastric secretions
(reduced peristalsis) 3.Ophthalmology: uveitis
4.Urinary urgency, urge
Contraindications: 2.CNS effects: incontinence, urinary
1.Glaucoma -Sedation (depression of frequency and/or nocturia
2.Prostatic cholinergic activity) (symptoms resulting from,
hyperplasia -Reduced tremor in Parkinson e.g., overactive bladder
disease syndrome)
Adverse effects: -Correct vestibular 4.Antidote for
1.Restlessness disturbances (blockade of anticholinesterase
-irritation,disorienta muscarinic receptors prevents poisoning: atropine
tion motion sickness) reverses the muscarinic
2.Blurred vision, effects of cholinergic
increased poisoning (e.g.,
intraocular pressure bronchoconstriction) but
3.Inhibition of does not reverse the
sweating (fever) nicotinic effects (e.g.,
4.Arrhythmias, muscle weakness,
cutaneous paralysis).
vasodilation 5.Scorpion stings
(Atropine flush)
5.Dry
mouth,constipation Scopolamine, 1.decrease ↓ Vestibular 1.Motion sickness
6.Urinary retention Benztropine disturbances (antiemetic) 2.Parkinson disease
(In patients with
large prostate) Tropicamide 1.Mydriasis Ophthalmology
2.Impaired accommodation 1.Therapeutic use: in
patients with uveitis
2.Diagnostic use: pupillary
dilation to allow ocular
fundus examination and
cycloplegia to allow
refractory testing
 Pirenzepine 1.Selective M1 1.It decreases gastric acid 1.Peptic ulcer disease
tertiary amine secretion through preferential
antimuscarinic action on gastric mucosa; also
reduces pepsin secretion

Quaternary amines Ipratropium 1.Bronchodilation 1.Chronic obstructive

Hydrophilic (poor (Competitive inhibition of pulmonary disease (COPD)
oral bioavailability muscarinic receptors prevents
and CNS bronchoconstriction.) 2.Bronchial asthma
penetration)

Contraindications:
1.Glaucoma
2.Prostatic
hyperplasia

Adverse effects:
1.Restlessness
-irritation,disorienta
tion
2.Blurred vision,
increased
intraocular pressure
3.Inhibition of
sweating (fever)
4.Arrhythmias,
cutaneous
vasodilation
(Atropine flush)
5.Dry
mouth,constipation
6.Urinary retention
(In patients with
large prostate)

Botulinum 1.Blocks the 1.Poisoning presets with 1.Localised injections of

toxin release of progressive paralysis, blurred BTX are used to treat
Acetylcholine vision, dysphagia(difficulty blepharospasm (blinking or
swallowing), dysarthria other eyelid movements,
(difficulty speaking), like twitching, that you can't
respiratory paralysis control), skin wrinkles
Neuromuscular blockers

Class Drugs MOA Effect Indication (use of that drug

for treating a particular
disease)

Non depolarizing d-Tubocurarine Onset of action: 1.Bind to Nm receptor For prolonged procedures
Neuromuscular Slow >5 min and prevent Ach receptor 1.Muscle relaxation during
blockers Duration of action:Long binding (compete with surgery
(Competitive (1-2 hours) Ach) 2.Assisted ventilation
antagonists of Metabolism:Liver 2.Inhibit the channel
NM receptors) ADRs: opening and Na+ influx
-Hypotension 3.Block the muscle
-Histamine release action potential
-Bronchospasm 4.The ACh antagonism is
surmountable by
increasing concentration
Pancuronium Onset of action: of Ach in vitro or
Intermediate (2-3min) anticholinesterase
Duration of action:Long (neostigmine)
Metabolism: Liver 5.Cause muscle paralysis
ADRs: 6.Consciousness and
-Less risk of hypotension pain are not affected
-Tachycardia 7.Some effects:
-Extrinsic eye
muscles(double vision)
Vecuronium Onset of action: -Facial muscles
Intermediate -Limbs and pharynx
Duration of action: (difficulty in
Intermediate (30-40 min) swallowing)
Metabolism:Liver -Respiratory muscles
ADRs: Less adrs

Rocuronium Onset of action: Fast

Duration of
action:Intermediate
(30-40 min)
Metabolism:Liver
ADRs: Less Adrs

Depolarizing Suxamethonium Phase 1: 1.Consciousness and Used for short procedures:

blockers chloride -Twitching of muscles pain sensation are not 1.Facilitation of intubation
(Agonists of NM (Succinylcholine) (fasciculation) and spasm affected 2.Laryngoscopy,
receptors) -Succinylcholine binds to 2.Short acting affect (5-8 bronchoscopy
Nm receptor and open mins) 3.Short orthopedic
channels like ACh 3.Succinylcholine is manipulations
-Cause Na influx and AP metabolized by plasma 4.Adjunct to
(initial depolarization) cholinesterase electroconvulsive therapy
4.Anticholinesterase
Phase 2: drugs do not overcome
-Paralysis the effect and even
-Does not get metabolised increase the duration of
by acetylcholinesterase action
-slowly dissociates from
receptor
-Na+ channels get
inactivated
-Acetylcholine release
cannot generate new AP

Spasmolytics (Act both centrally and peripherally, decreases muscle tone without reducing voluntary power)

Class Drugs MOA Effect Indication (use of that

drug for treating a
particular disease)

Centrally acting Diazepam 1.Binds to GABA 1.Spastic neurological

receptors in CNS diseases (hemiplagia,
2.Enhances GABA paraplegia,spinal injuries,
transmission which cerebral palsy, multiple
inhibits CNS and leads to: sclerosis)
-muscle relaxation 2.Tetanus
(muscle tone is reduced 3. Epilepsy
mostly at supraspinal 4. Electroconvulsive
level) therapy
-anticonvulsant 5. Orthopedic
-sedation manipulations
-hypnotic effect 6.Anxiety and tension
-antianxiety (anxiolytic
effect)

Tizanidine 1.Central a2 agonist ADRs: 1.Spastic neurological

(similar to clonidine) 1.Hypotension diseases (hemiplagia,
-inhibits release of 2.Dry-mouth paraplegia, spinal injuries,
excitatory amino acids in 3.Drowsiness cerebral palsy, multiple
the spinal interneurons 4.Insomnia sclerosis)
 2. Reduces muscle tone
and spasm without
muscle strength

Baclofen 1.Analogue of GABA and ADRs: 1.Used in treatment of

(spinal cord) activates GABAb 1.Sedation spasticity in multiple
receptors 2.Somnolence sclerosis or spinal cord
2.Primary site of action is 3.Slurred speech lesions
the spinal cord where it 4.Hypotension
depresses muscle tone
reflexes
-Less sedative than
diazepam

Peripherally Dantrolene 1.Acts on the ADRs: 1.Spastic

acting RyR(Ryanidue receptor) 1.Severe muscular syndrome(cerebral palsy,
calcium channels in the weakness (is used only multiple sclerosis, spinal
SPR of skeletal muscles for non ambulatory cord injury, stroke)
and prevents their patients) 2.Malignant hyperthermia
opening and release 2.Hepatotoxicity 3.Neuroleptic malignant
calcium 3.Crosses BBB and syndrome
2.Decreases intracellular causes sedation and other
calcium concentration CNS effects (respiratory
3.Causes muscle depression, drowsiness,
relaxation and reduces blurred vision)
spasticity with loss of
voluntary power

Botulinum 1.Block Ach release and ADRs: 1.Different muscle spasms

Toxin diminish activity of 1.May cause respiratory -Strabismus
parasympathetic paralysis from -Blepharospasm
cholinergic synapses unexpected spread from -Spasticity associated with
the site of injection cerebral palsy (pediatrics)
2.Produce flaccid 2.Risk of anaphylaxis or stroke (adults)
paralysis of skeletal
muscles 2.Hyperhidrosis
3.Sialorrhea
3.Inhibition lasts 3-4 4.Cosmetics
months -Facial wrinkles

4.Is used locally

(Intramuscular or
intradermal injections)