drug receptors & pharmacodynamics
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Drug Receptors &
Pharmacodynamics
Nancy Bruton-Maree, CRNA, MS
Raleigh School of Nurse Anesthesia
UNCG
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Pharmacodynamics
The component of a cell or organism that interactswith a drug & initiates the chain of events leading tothe drugs observed effect is a receptor
Receptors have become the central focus ofinvestigation of drug effects & their mechanisms ofaction (Pharmacodynamics)
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Receptor Concept
Receptors largely determine the quantitativerelations between dose or concentration of drug &pharmacologic effects
Receptors are responsible for selectivity of drugaction
Receptors mediate the actions of pharmacologicagonists & antagonists
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Common Definitions
Orphan receptors their ligands have not beenidentified
Regulatory proteins Proteins which medicate theactions of endogenous chemical signals
Classes of proteins
Enzymes one of the types of receptors that has been identifiedwhich may be inhibited by binding a drug
Transport proteins
Structural proteins
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Relation Between Drug Concentration &Response
This can be described with mathematical precision This is an idealized relationship that underlies the
more complex relations between dose & effect thatoccur when a drug is given to a patient.
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Concentration-Effect Curve & ReceptorBinding of Agonists
Responses to low doses of a drug usually increasein direct proportion to dose
As doses increase, the response incrementdiminishes
Doses may be reached at which no further increasein response can be achieved
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Equation Used to Develop Curve
E = Emax X C C + EC50
E = effect observed at concentration C
EMAX = the maximal response that can be producedby the drug
EC50 = the concetration of drug that produces 50%of maximal effect
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Relationship Between Drug Concentration& Drug Effect or Receptor Bound Drug
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The Drug Concentration at Which Effect or ReceptorOccupancy is Half-Maximal Are Denoted by EC50 & Kd
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Hyperbolic Relationship
Resembles the mass action law, which describesassociation between 2 molecules of a given affinity
This resemblance suggests that drug agonists actby binding to a distinct class of biologic moleculeswith a characteristic affinity for the drug receptor
Drug bound to receptors (B) relates to theconcentration of free (unbound) drug (C) as
depicted in the previous slide
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Previous Curve
Equation B = Bmax X C C + Kd Bmax = indicates the total concentration of receptor sites
Kd = the concentration of free drug at which half-maximalbinding is observed. This constant characterizes thereceptors affinity for binding the drug in a reciprocal
fashion
If the Kd is low, the binding affinity is high and vice versa
The EC50 & Kd may be identical, but need not be
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Other Facts About Curves
Dose-response data are often presented as a plotof the drug effect (ordinate) against the logarithm ofthe dose or concentration (abscissa)
This makes the curve sigmoid in shape with a linearmidportion
This expands the scale of the concentration axis atlow concentrations (where the effect is changing
rapidly) & compresses it at high concentrations(where the effect is changing slowly), but has nospecial biologic or pharmacologic significance.
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Receptor-Effector Coupling & SpareReceptors
Coupling the transduction process that links drugoccupancy of receptors & pharmacologic response
The relative efficiency of occupancy-responsecoupling is partially determined by the initialconformational change in the receptor
The effect of full agonists can be considered moreefficiently coupled to receptor occupancy than can
the effects of partial agonists
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Receptor-Effector Coupling & SpareReceptors
Receptor occupancy into cellular response couplingefficiency is also determined by the biochemicalevents that transduced
Sometimes the biologic effect of the drug is linearlyrelated to the number of receptors bound
This is often true for the drug-regulated ionchannels in which the ion current produced by the
drug is directly proportional to the number ofreceptors bound
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Receptor-Effector Coupling & SpareReceptors
Factors that contribute to non-linear occupancy-response coupling
spare receptors receptors are spare for a givenpharmacologic response if it is possible to elicit a
maximal biologic response at a concentration of agonistthat does not result in occupancy of the full complementof available receptors
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Receptor-Effector Coupling & SpareReceptors
What does Temporal mean? Maximal response can be elicited by activation of relatively
few receptors because the response initiated by an individualligand-receptor binding event persists longer than the bindingevent itself
Spare in number If the concentration or amount of cellularcomponents other than the receptors limits the coupling ofreceptor occupancy to response, then a maximal responsecan occur without occupancy of all receptors; thus thesensitivity of a cell or tissue to a particular concentration of
agonist depends not only on the affinity of the receptor forbinding the agonist but also on the degree of spareness (thetotal number of receptors present compared with the numberactually needed to elicit a maximal response.
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Receptor-Effector Coupling
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Concept of Spare Receptor Coupling
B Bmax = C C + Kd
The Dd of the agonist-receptor interaction
determines what fraction (B/Bmax) of total receptorswill be occupied at a given free concentration (C) ofagonist regardless of the receptor concentration
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Competitive & Irreversible Antagonists
Receptor antagonists bind to receptors but do notactivate them
The primary action of antagonists is to preventagonists from activating receptors
Inverse agonist also an antagonist but can reducereceptor activity below basal levels observed in theabsence of bound ligand
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Competitive & Irreversible Antagonists
Competitive Antagonist In the presence of a fixedconcentration of agonist, increasing concentrations of areversible antagonist progressively inhibit the agonistresponse
High antagonist concentration prevent response completely. However, sufficiently high concentrations of agonist can
surmount the effect of a given concentration of theantagonist.
Because the antagonism is competitive, the presence ofantagonist increases the agonist concentration required fora given degree of response and so the agonistconcentration-effect curve is shifted to the right.
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Competitive Antagonism
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Competitive v. Irreversible Antagonism
The concentration of the agonist required toproduce a given effect in the presence of a fixedconcentration of competitive antagonist is greaterthan the concentration of the agonist required to
produce the same effect when the antagonist is notpresent.
The ratio of the two agonists concentration is
related to the dissociation constant of theantagonist by the Schild equation
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Noncompetitive Antagonist
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Schild Equation
C C = 1 + [I] Ki
C is the concentration of an agonist required to produce agiven effect in the presence of a fixed concentration [I] of
competitive antagonist
[I] is the fixed concentration of the antagonist
C the agonist concentration required to produce the sameeffect in the absence of the antagonist
Ki is the dissociation constant of the antagonist
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Importance of Schild Equation
The degree of inhibition produced by a competitiveantagonist depends on the concentration ofantagonist
Clinical response to a competitive antagonistdepends on the concentration of agonist that iscompeting for binding to receptors
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Irreversible Antagonism
This type of antagonism may be irreversible ornearly irreversible
It involves forming covalent bonds or binding sotightly to receptors that the receptor is unavailableto the agonist
P ibl R l f I ibl
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Possible Reversal of IrreversibleAntagonism
Ad t & Di d t f I ibl
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Advantages & Disadvantages of IrreversibleAntagonism
Once the irreversible antagonist has occupied thereceptor, it need not be present in unbound form toinhibit agonist responses
Therefore, the duration of action of such anirreversible antagonist is relatively independent ofits own rate of elimination & more dependent on therate of turnover of receptor molecules
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Noncompetitive Antagonists
Noncompetitive antagonists can function in differentways:
By binding to a site on the receptor protein separate fromthe agonist binding site which prevents receptor
activation without blocking agonist binding Although these drugs can act noncompetitively, their
action is reversible if they do not bind covalently
Allosteric modulators function without inactivating the
receptor & alter receptor function without inactivating thereceptor
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Partial Agonists
There are two classes of agonists based on themaximal pharmacologic response that occurs whenall receptors are occupied.
The two classes are full agonist & partial agonist
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Receptor-Effector Coupling
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Partial Agonist v. Full Agonist
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Partial Agonists
Facts Failure of a partial agonist to produce a maximal
response is not due to decreased affinity for bindingreceptors
Partial agonists competitively inhibit the responsesproduced by full agonists
Many drugs used as antagonists are actually weak partialagonists
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Partial Agonist
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Other Mechanisms of Drug Antagonism
Chemical antagonist one drug acts as a chemicalantagonist of the other simply by ionic binding that makesthe other drug unavailable for interactions with the proteinsinvolved in the outcome (i.e., blood clotting)
Physiologic antagonist between endogenous regulatorypathways mediated by different receptors. The use ofphysiologic antagonists produces effects that are lessspecific & less easy to control than are the effects of areceptor-specific antagonism
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Signaling Mechanisms & Drug Action
Questions to answer: Why do some drugs produce effects that persist for minutes, hours,
or even days after the drug is no longer present in the body?
Why do responses to other drugs rapidly diminish with prolonged orrepeated administration?
How do cellular mechanisms for amplifying external chemical signalsexplain the phenomenon of spare receptors?
Why do chemically similar drugs often exhibit extraordinaryselectivity in their actions?
Do these mechanism provide targets for enveloping new drugs?
Five Basic Mechanisms of Transmembrane
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Five Basic Mechanisms of TransmembraneSignaling
Lipid-soluble ligand that crosses the membrane & acts as anintracellular receptor
Transmembrane receptor protein whose IC enzymatic activity isallosterically regulated by a ligand that binds to a site on theproteins EC domain
Transmembrane receptor that binds & stimulates a proteintyrosine kinase
Ligand-gated transmembrane ion channel that can be induced toopen or close by the binding of ligand
Transmembrane receptor protein that stimulates a GTP-bindingsignal transducer protein (G protein)which in turn modulatesproduction of an IC second messenger.
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Five Basic Mechanism
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IC Receptors for Lipid-Soluble Agents
Classes include: Steroids
Thyroid hormone
The receptors for these stimulate transcription ofgenes by binding to response elements on DNAnear the gene whose expression is to be regulated
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IC Receptors
Two Therapeutically Important
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Two Therapeutically ImportantConsequences
All of these hormones produces their effect after acharacteristic lag period of 30 minutes to severalhours
The time required to synthesize new proteins
The effects of these agents can persist for hours ordays after the agonist concentration has beenreduced to zero
The persistence is due to slow turnover of mostenzymes & proteins, which can remain active in cells forhours or days after synthesis.
Ligand Regulated Transmembrane Enzymes
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Ligand-Regulated Transmembrane EnzymesIncluding Receptor Tyrosine Kinases
Signalling is by trophic hormones Examples are insulin, epidermal growth factor (EGF),
platelet-deriving growth factor (PDGF), atrial natriureticpeptide (ANP), & transforming growth factor- (TGF-)
Receptors are polypeptides consisting of an EC hormone-binding domain & a cytoplasmic enzyme domain
May be a protein tyrosine kinase, a serine kinase, or aguanylyl cyclase
The two domains are connected by a hydrophobic segmentof the polypeptide that crosses the lipid bilayer of theplasma membrane
Ligand-Regulated Transmembrane
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Ligand-Regulated TransmembraneEnzymes
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What Limits Intensity & Duration of Action
Down-regulation occurs when tyrosine kinasesare involved
Ligand-binding induces accelerated endocytosis ofreceptors from the cell surface, followed by the
degradation of receptors from the cell surface.
When this process occurs at a rate faster than denovo synthesis of receptors, the total number of
cell-surface receptors is reduced.
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Cytokine Receptors
Phosphorylated tyrosine residues on the receptorscytoplasmic surface then set in motion a complexsignaling dance by binding another set of proteins,called STATs
The bound STATs are themselves phosphorylatedby the JAKs, 2 STAT molecules dimerize theSTAT/STAT dimer dissociates form the receptor &
travels to the nucleus, where it regulatestranscription of specific genes.
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Cytokine Receptors
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Ligand- and Voltage-Gated Channels
Natural ligands are Acetylcholine
Serotonin
GABA
Glutamate
Each of their receptors transmits its signal acrossthe plasma membrane by increasing
transmembrane conductance of the relevant ion &thereby altering the electrical potential across themembrane
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Ligand- & Voltage-Gated Receptors
The time elapsed between the binding of the agonist to aligand-gated channel & the cellular response can often bemeasured in milliseconds
Ligand-gated ion channels can be regulated by multiple
mechanisms, including phosphorylation and endocytosis Voltage-gated channels do not bind neurotransmitters
directly but are controlled by membrane potential
Such channels are also important drug targets
G C
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Ligand- & Voltage-Gated Channels
G P i & S d M
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G Proteins & Second Messengers
Second messengers are cyclic adenosine-3,5 -monophophate (cAMP), calcium ion, &phophoinositides
G proteins usually use a transmembrane signaling
system with 3 separate components
EC ligand
Receptor
Activated G protein The concentration of second messenger changes
G P i & S d M
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G Protein & Second Messenger
For cAMP, the effector enzyme is adenylyl cyclase Examples of G protein receptors
adrenoceptors
Glucagon receptors
Thyrotropin receptors
Dopamine receptors
Serotonin receptors
G P t i & S d M
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G Protein & Second Messenger
Duration of activation of adenylyl cyclase dependson the longevity of GTP binding to the G protein
Receptors coupled to G proteins are GPCRs
They make up a family of seven-transmembrane(7TM) or serpentine receptors
G P t i & S d M
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G Proteins & Second Messengers
G P t i & S d M
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G Proteins & Second Messenger
GPCRs exist as homodimers & heterodimers
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R t R l ti D iti ti
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Receptor Regulation - Desensitization
R t R l ti D R l ti
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Receptor Regulation Down Regulation
Well Established Second Messengers
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Well Established Second Messengers
cAMP Calcium & Phophoinositides
cGMP
cAMP Second Messenger Pathway
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cAMP Second Messenger Pathway
Calcium & Phosphoinositides
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Calcium & Phosphoinositides
Some of the hormones, neurotransmitters, &growth factor that trigger this pathway bind toreceptors liked to G proteins; others bind toreceptor tyrosine kinases
Crucial step is stimulation of a membrane enzyme,phospholipase C which splits a minor phospholipidcomponent of the membrane, phophatidylinosital-4,5-bisphophate, into 2 second messengers,diacylglycerol and inositol-1,4,5-trisphosphate
Ca2+ Phosphoinositide Signaling Pathway
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Ca2+ -Phosphoinositide Signaling Pathway
Cyclic Guanosine Monophosphate
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Cyclic Guanosine Monophosphate
cGMP establishes signals in only a few cells Cell-surface receptors stimulate membrane-bound
guanylyl cyclase to produce cGMP
cGMP acts by stimulating a cGMP-dependentprotein kinase
Termination is by enzymatic degradation of thecyclic nucleotide & by phosphorylation of kinase
substrates
cGMP
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cGMP
Interplay Among Signaling Mechanisms
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Interplay Among Signaling Mechanisms
Calcium-phosphoinositide & cAMP signalingpathways oppose one another in some cells butcompliment each other in other cells
Phosphorylation
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Phosphorylation
Supplies amplification & flexible regulation Amplification the attachment of a phosphoryl
group to a serine, threonine, or tyrosine residuepowerfully amplifies the initial regulatory signal by
recording a molecular memory that the pathwayhas been activated
Dephosphorylation erases the memory
Phosphorylation
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Phosphorylation
Flexible regulation differing substrate specificitiesof the multiple protein kinases regulated by secondmessengers provide branch points in signalingpathways that may be independently regulated
Receptor Classes & Drug Development
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Receptor Classes & Drug Development
Structure-activity relationship the agonist orantagonist that occupies the same receptor as theagonist must fit the receptor like a lock & key
If two agonists exhibit identical relative potencies in
producing 2 distinct effects, it is likely that the 2effects are mediated by similar or identical receptormolecules
The same neurotransmitter can act on differentreceptor types
Dose & Response In Patients
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Dose & Response In Patients
Graded Dose-Response Relationships to chooseamong drugs & to determine appropriate doses of adrug, one must know
Pharmacologic potency
Maximal efficacy
In relation to the desired therapeutic effect wanted
Graded Dose-Response Curves
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Graded Dose-Response Curves
Potency
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Potency
Refers to the concentration (EC50 ) or dose (ED50 )of a drug required to produce 50% of that drugs
maximal effect
Potency determines the administered dose of drug
Potency depends in part on
Affinity of receptors for binding the drug
The Efficiency with which drug-receptor interaction is
coupled to response
Potency
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Potency
Potency of a drug should be stated in dosage units Relative potency, the ratio of equi-effective doses,
may be used in comparing 2 drugs
Efficacy
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Efficacy
A drugs clinical effectiveness depends not on itspotency but on it maximal efficacy & its ability toreach the relevant receptors
This can depend on
Its route of administration
Absorption
Distribution
Clearance from blood
Clearance from its site of action
Maximal Efficacy
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Maximal Efficacy
Efficacy is shown on the response axis The drugs propensity to cause toxic effects may
limit the ability to utilize its maximal efficiacy
Efficacy may be determined by
The drugs mode of interactions with the receptors
By characteristics of the receptor-effector systeminvolved
Graded Dose-Response Curves
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Graded Dose Response Curves
Shape of Dose-Response Curves
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Shape of Dose Response Curves
Curves A, B, & C in the preceding slide approximate theshape of a simple Michaelis-Menton relation. Not all clinicalresponses do this
Extremely steep dose-response curves like curve D mayhave important clinical consequences if the upper portion ofthe curve represents an undesirable extent of response
Steep dose-response curves can result from cooperativeinteractions of several different actions of a drug
Quantal Dose-Effect Curves
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Quantal Dose Effect Curves
These curves determine the dose of drug requiredto produce a specified magnitude of effect in alarge number of patients or experimental animals
They plot the cumulative frequency distribution of
responders v. the log dose
A specific quantal effect may be chosen on thebasis of clinical relevance, for preservation of safety
of experimental subjects, or it may be an inherentlyquantal event
Quantal Dose-Effect Curves
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Quantal Dose Effect Curves
The frequency distribution of such responses areplotted against the log of the dose, which producesa gaussian normal curve variation
When these responses are summated, the resulting
cumulative frequency distribution constitutes aquantal dose-effect curve or the proportion orpercentage of individuals who exhibit the effectplotted as a function of log dose
Quantal Dose-Effect Curve
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Quantal Dose Effect Curve
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Both curve types give information about potency &selectivity of drugs
Graded dose-response curves indicate maximalefficacy of a drug
Quantal dose-effect curves indicate potentialvariability of responses among individuals
Variation In Drug Responsiveness
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Variation In Drug Responsiveness
Idiosyncratic drug responses
Idiosyncratic responses
Immunologic mechanisms (hypersensitivity)
Quantitative variations
Hyporeactive
Hyperreactive Tolerance
Tachyphylaxis
Need to consider:
Propensity of a drug to produce tolerance or tachyphylaxis Effects of sex, age, body size, disease states, genetic factors,
simultaneous administration of other drugs
Four Mechanisms That Contribute ToV i ti I D R
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Variation In Drug Response
Alteration in concentration of drug that reachesreceptor
Variation in concentration of an endogenousreceptor ligand
Alterations in number or function of receptors
Changes in components of response distal to thereceptor
Clinical Selectivity: Beneficial v. ToxicEff t f D
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Effects of Drugs
Beneficial & toxic effects mediated by the samereceptor-effector mechanism
Beneficial & toxic effects mediated by identicalreceptors but in different tissues or by different
effector pathways Beneficial & toxic effects mediated by different
types of receptors
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