BMS 123 · Common Core (Tronc commun)Section 6.4 · Dose–response, interactions and variability
Section 26 of 27
Types of antagonism
Name and distinguish pharmacodynamic, chemical, physiological and pharmacokinetic antagonism, with an example of each.
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Why this matters
Not every loss of drug effect is a blocked receptor. Sometimes two drugs react in the same syringe, sometimes they pull the body in opposite directions, and sometimes one drug simply removes the other from the body before it can act. The four types of antagonism are the vocabulary that lets you say which is happening. Without it, an unexpected loss of effect is a mystery; with it, you can look in the right place, and you can also recognise which interactions are wanted therapy and which are accidents to prevent.
What you need to know first
You need the receptor vocabulary of Unit 5.5 and the competitive and non-competitive curves of Unit 6.3. Unit 3.4 (enzyme induction) and Unit 4.2 (urinary pH) are useful background for the pharmacokinetic type.
Words to know (5)
Pharmacodynamic antagonism
Antagonism in which an administered drug blocks the receptor of an endogenous or administered agonist. An antagonist occupying the same receptor as a hormone reduces the hormone’s effect.
Chemical antagonism
A simple chemical reaction between two or more drugs that leads to loss of activity. Dimercaprol reduces heavy-metal toxicity by chelating the metal.
Physiological antagonism
Two drugs act on different receptors to produce opposite physiological effects that cancel each other. Histamine dilates vessels while adrenaline constricts them, so the two oppose each other.
Pharmacokinetic antagonism
Antagonism occurring during absorption, distribution, metabolism or excretion, so less active drug reaches the site of action. Phenobarbitone accelerates the hepatic metabolism of warfarin and lowers its effect.
Drug–drug interaction
A change in the effect of one drug caused by another drug given at the same time; the change may be intended or unwanted. An antibiotic that lowers the effect of an oral contraceptive is an unwanted interaction.
One idea at a timeIdea 1 / 4
In one sentence Pharmacodynamic antagonism occurs between an administered antagonist and an endogenous agonist competing at the same receptor.
Pharmacodynamic antagonism happens at the receptor
Pharmacodynamic antagonism, also called receptor-blockade antagonism, occurs between an administered antagonist and an endogenous ligand acting as an agonist. The antagonist occupies the receptor, so the natural messenger cannot activate the cell; the effect depends on the relative concentrations of both substances at that receptor. It is the type described in Unit 6.3, where the shape of the displaced curve distinguishes a competitive block, which can be surmounted by more agonist, from a non-competitive block, which cannot. Because the site of the conflict is the receptor itself, this is the antagonism most directly connected to the drug’s mechanism of action.
For example
An antagonist that occupies the same receptor as a hormone reduces the hormone’s effect even though the hormone is still being released normally.
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Where does pharmacodynamic antagonism take place?
Show the answer
At the receptor itself: the administered antagonist occupies the binding site and prevents the endogenous agonist from activating the cell, so the two compete for the same target.
Read detailed explanations
Interactions that reduce effect: from intended antidotes to avoidable harm
A drug–drug interaction is any change in the effect of one drug caused by another, and the four types of antagonism describe its mechanisms rather than its desirability. Some are deliberately created. Chelation therapy, the use of an antagonist to reverse a poisoning, and the use of a physiological antidote such as a vasoconstrictor against a vasodilator are all antagonism put to work. Others are accidents of co-prescription. The practical problem is that the same mechanism can serve both purposes, and the clinician has to decide which is present. Consider a patient whose anticoagulant effect falls after a new drug is started. If the new drug induces the enzymes that metabolise the anticoagulant, the response is pharmacokinetic: the anticoagulant concentration falls, and the safest action is to reconsider the combination rather than to raise the dose, because stopping the inducing drug later will send the concentration back up. If instead the new drug displaces the anticoagulant from plasma protein or competes at a receptor, the concentration of active drug or the response at the target changes in a different way. The epidemiology matters too: the more medicines a patient takes, the greater the number of possible pairs, which is why polypharmacy in older patients is a major source of interactions. Some interactions are predictable from the mechanism, such as enzyme induction or the chelation of metal ions, and can be anticipated before the first dose; others appear only when a patient with an unusual combination of disease and drugs is exposed, and are found by vigilance rather than by memory. The skill being taught is not a list to memorise but a set of questions: what does the other drug do to absorption, to metabolism, to excretion, to the receptor, and to the opposing system?
Antagonism applied: reversal, rescue and prevention
Antagonism is not only something to avoid; it is a therapeutic tool whose design follows the mechanism. Competitive antagonism is the basis of reversible reversal: an opioid receptor antagonist binds the same receptor as the opioid and, because it competes with higher affinity, it restores breathing in opioid overdose. The same principle explains why a competitive block can be overcome by a surge of the body’s own agonist, which is why some blocks fail as the patient’s condition changes. Non-competitive antagonism is used when permanence is wanted rather than reversibility: an irreversible inhibitor that disables an enzyme in a parasite or a tumour cell keeps working after the drug has been cleared, so the duration of action exceeds the drug’s presence. Chemical antagonism supplies the antidotes that work by binding rather than by blocking, such as a chelator holding a metal ion in an excretable complex, and it also supplies the dispensing rule that two oppositely charged drugs must not share a syringe. Physiological antagonism is the basis of support-the-opposing-system treatment: when a mediator causes vasodilatation and bronchoconstriction, the natural temptation is to block the mediator’s receptor, yet adrenaline can rescue the patient immediately by acting on other receptors with the opposite effects. Each strategy carries its own failure mode. A competitive antagonist can be out-competed, a non-competitive one makes the effect difficult to adjust, a chelator may also remove useful metal ions, and a physiological antagonist may push the system so far in the other direction that it creates a new problem. Reading the mechanism before acting is what separates rational reversal from guessing.
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Where antagonism can happen
Four doors lead to the same result — a smaller effect — but they open at the receptor, in the syringe, on a second receptor system, or in the pharmacokinetic handling of the drug.
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01 / 4Pharmacodynamic antagonism
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Pharmacodynamic antagonism
An administered drug occupies the same receptor as the agonist and prevents it from activating the cell. The effect depends on the concentrations of both drugs at that receptor, which is why adding more agonist can overcome a competitive block but not an irreversible one.
Schematic, not to scale. Real interactions often combine mechanisms: a single pair of drugs may be antagonistic at the receptor and also change the other drug’s metabolism, so the net effect must be judged for the individual patient.
Key points to remember
✓Pharmacodynamic antagonism occurs at the receptor between an administered antagonist and an endogenous agonist.
✓Chemical antagonism is a direct chemical reaction that destroys activity, as when dimercaprol chelates a heavy metal or a penicillin and an aminoglycoside precipitate in one syringe.
✓Physiological antagonism uses two different receptors with opposite effects, as with histamine and adrenaline.
✓Pharmacokinetic antagonism acts on absorption, metabolism, distribution or excretion, as when phenobarbitone accelerates the metabolism of warfarin.
✓All of these are drug–drug interactions, and they may be intended therapy or unwanted harm.
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Worked example
Classifying four interactions. Four situations are reported on a ward round. (1) A chelating agent is given for lead poisoning. (2) A penicillin and an aminoglycoside are drawn into the same syringe. (3) Histamine lowers blood pressure in a patient who then receives adrenaline. (4) A patient on warfarin starts phenobarbitone and the anticoagulant effect falls. Name the type of antagonism in each case and say where the conflict happens.
Case 1: chemical antagonism. The chelator binds the metal directly and the toxic species loses its activity; the conflict is a chemical reaction in the body, with no receptor involved.
Case 2: also chemical antagonism, but it happens in vitro. The opposite charges of the penicillin and the aminoglycoside form an insoluble precipitate before administration, so the practical response is to give the injections separately.
Case 3: physiological antagonism. Adrenaline acts on different receptors from histamine and produces the opposite vascular effect, so the effects cancel at the level of the tissue rather than at one receptor.
Case 4: pharmacokinetic antagonism at the level of metabolism. Phenobarbitone induces the hepatic enzymes that remove warfarin, so the concentration reaching the site of action falls; the receptor is untouched and the answer is to review the combination.
Check whether each interaction was intended. The chelator is therapeutic, separating the injections is preventive practice, the adrenaline is a deliberate physiological antidote, and the warfarin interaction is an unwanted consequence to be avoided.
Naming the type of antagonism is not a vocabulary exercise: it tells you where to look. Receptor, syringe, tissue or pharmacokinetics — and once you know where, you know whether the fix is another drug, a change in administration, or a change in the treatment plan.
Common misconception
Beginners often treat antagonism as synonymous with receptor blockade, so they look for a blocked receptor in every case. In physiological antagonism the receptors are all working normally, and in chemical and pharmacokinetic antagonism no receptor is involved at all: the drug is inactivated, pushed in the opposite direction, or removed from the body before it can act.
Check your reasoning
Give one reason why a clinician must distinguish pharmacokinetic from pharmacodynamic antagonism when a drug seems to stop working.
Reveal an answer
Because the corrective action is different. In pharmacodynamic antagonism the problem is at the receptor, so a higher agonist concentration or a different antagonist may help; in pharmacokinetic antagonism the drug is being removed faster, so the answer may be to stop the interacting drug, adjust the dose interval or change the route rather than to increase the dose blindly.
Where this comes from
BMS 123 General Pharmacology II lecture notes, Part 2 — Principles of Pharmacodynamics · Unit 3.4.4, Other types of antagonism: chemical, physiological and pharmacokinetic antagonism
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About this course and its sources
Bilingual lessons organised from the supplied BMS 123 General Pharmacology II lecture notes (Principles of Pharmacokinetics and Principles of Pharmacodynamics). Diagrams are original educational schematics; pharmacology, nursing and French-language review are pending.