This document discusses different types of receptors including ligand gated ion channels, G-protein coupled receptors, enzyme linked receptors, and nuclear receptors. It describes receptor-drug interactions including affinity, intrinsic activity, efficacy, and potency. It defines different types of agonism and antagonism. The document provides examples and details on various receptor types and their mechanisms of action. In conclusion, extensive receptor pharmacology research has led to new drug targets, but more remains to be discovered about new receptor types and orphan receptors to further advance treatment options.

1. Receptor
pharmacology
Submitted By-
SHWETA TYAGI
M.PHARM – 1st YEAR
DEPARTMENT OF
PHARMACEUTICAL
TECHNOLOGY
MIET

2. TYPES OF RECEPTORS
.Ligand Gated Ion Channels
.G-Protein Coupled receptors
.Enzyme Linked receptors
.Nuclear receptors

3. WHAT IS DRUG
Drug is any substance or product that is
used for diagnosis, prevention,
treatment/cure of a disease or is intended to
be used to modify or explore physiological
systems or pathological states for the
benefit or to promote well being .

4. DRUG RECEPTOR
INTERACTIONS
 LIGAND: Any molecule which attaches
selectively to particular receptor
 AFFINITY: Capability of drug to bind to
the receptor and form receptor complex
 INTRINSIC ACTIVITY: Ability of the
drug to trigger the pharmacological response
after forming complex

5. DETERMINANTS OF DRUG
ACTIVITY
Efficacy: The ‘strength’ of the agonist receptor
complex in evoking a response of the tissue
Potency: Amount of drug needed to produce an
effect .

6. RECEPTOR THEORIES

7. AGONIST
A drug that binds to physiological receptor
and mimic the regulatory effects of
endogenous
substance.
It has high affinity and high intrinsic activity

9. TYPES OF AGONISM
Summation :- Two drugs eliciting same
response, but with different mechanism
and their combined effect
is equal to their summation.
Aspirin Codiene
PG Opoid receptor
Analgesic+ Analgesic+

10. Additive: combined effect of two drugs
acting by same mechanism.
Aspirin + NSAIDS

11. SYNERGISM (SUPRA
ADDITIVE):-
The combined effect of two drug effect is
higher than either individual effect.
1.Sulfamethaxazole+ Trimethoprim
2. Levodopa + Carbidopa

12. PARTIAL AGONIST
Full affinity + low intrinsic activity
Partly as effective as agonist
Greater affinity for RA than RI
Cannot produce a full biological
response at any concentration
ex: Pentazocine

13. INVERSE AGONIST
Full affinity & intrinsic activity<0(0 to-1) Inverse
agonists bind with the constitutively active
receptors, stabilize them, and thus reduce
the activity(negative intrinsic activity).
Eg. Beta carbolines on BZD receptor
Chlorpheneramine on H1,
Risperidone/clozapine/chlorpromazine on 5HT2a
Ziprasidone/olanzapine on 5-HT2c

15. ANTAGONIST
A drug is said to be an antagonist when it binds to
a receptor and prevents (blocks or inhibits) a
natural compound or a drug to have an effect
on the receptor. An antagonist has no activity.
Types of Antagonism
1. Chemical antagonism
2. Physiological /Functional antagonism
3. Pharmacokinetic antagonism
4. Pharmacological antagonism
Competitive ( Reversible/irreversible)
Non competitive (Irreversible)

16. LIGAND GATED ION
CHANNELIonotropic Receptors Typically receptors on
which fast neurotransmitters act
Timescale: Milliseconds
Localization: Membrane
Effector: Ion Channel
Coupling: Direct
Gating mechanism: conformational change
occurs in extracellular part of the receptor
Examples: Nicotinic Ach Receptor, GABA-A
Receptor,Glutamate Receptor, Glycine
receptor, 5–HT3, AMPA &

17. ION CHANNELS
These channels open when the cells
depolarised.They underlie the mechanism of
membrane excitability
Activation induced by membrane
depolarisation is short lasting, even if the
depolarisation is maintained
The most important channels in this group
are selective sodium, potassium or calcium
channelsl membrane .

19. G – PROTEIN –
COUPLED RECEPTORS
Largest family
Metabotropic or 7–Transmembrane/Heptahelical
(α-helices) receptors
Extracellular N-terminal domain and intracellular
Cterminal domain
3rd cytoplasmic loop couples to the G- Protein
Timescale : Seconds
Location : Membrane

20. Effector : Channel or Enzyme
Coupling : G- Protein
Examples : adrenoceptors, Muscarinic Ach,
histamine serotonin, opioid, cannabinoid,
amine, peptide, prostanoid receptors

22. TARGETS FOR G-
PROTEINS
.ADENYLATE CYCLASE

23. PHOSPHOLIPASE C/IP3/DAG

25. Ion Channels like K⁺ and Ca⁺⁺ channels are controlled
by direct interaction between the βγ-subunit of G0
and the channel
Phospholipase A2(formation of arachidonic acid and
eicosanoids)
Rho A/Rho kinase, a system that controls the
activity of many signaling pathways controlling cell
growth and
proliferation, smooth muscle contraction, etc.
Mitogen-activated protein kinase (MAP kinase),
activated by cytokines and growth factors acting on
kinase-linked
receptors and by GPCR ligands. Controls processes
involved in cell division, apoptosis and tissue
regeneration

26. ENZYME LINKED
RECEPTORLarge, heterogenous group responding
mainlyto protein mediators.
Timescale : Hours
Location : Membrane
Effector : Protein Kinases
Coupling : Direct
Examples : Insulin, Growth Factors, Cytokine,
ANF receptors

29. NUCLEAR RECEPTOR
. Two main categories:
1) Present in the cytoplasm, form homodimers
and migrate to the nucleus. Their ligands are
mainly endocrine in nature (e.g. steroid
hormones)
2) constitutively present in the nucleus and
from heterodimers with the retinoid X receptor.
Their ligands are usually lipids (e.g. fatty acids).
A third subgroup transduce mainly endocrine
signals but function as heterodimers with
retinoid X receptor (e.g thyroid harmone)

30. IN CYTOPLASM

31. IN NUCLEUS

32. CONCLUSION
Extensive research done on Receptor
pharmacology -lead to discovery of new drug
targets for treatment of several diseases.
Still requires discovery of new receptor types
and the mechanisms of many orpha receptors
that can result in effective treatment of many
diseases.
Requires development of receptor
crystallization etc.
Much to be discovered about the nuclear
receptors

33. REFERENCE
1 . K.D Tripathi