Pharmacodynamics: receptors and signalling !

What a drug does to the body: the molecular targets drugs bind, the signals they set off, and why responses fade with repeated use.

Updated 2026-11-01

Pharmacodynamics studies how drugs produce their effects. Most drugs bind a protein target (a receptor, enzyme, ion channel or transporter) and change its activity. Receptors fall into a few families that differ in speed and in the signals they send, and the body adapts to repeated stimulation, which explains tolerance.

Receptor families

Ligand-gated ion channels: nicotinic acetylcholine receptor, GABA-A receptor; binding opens a pore and ions flow
G protein-coupled receptors (seven transmembrane segments): adrenergic, muscarinic, opioid receptors; signal through Gs (cAMP up), Gi (cAMP down) or Gq (calcium up)
Enzyme-linked receptors: the insulin receptor is a tyrosine kinase
Intracellular receptors: steroid and thyroid hormones cross the membrane and act on DNA, so effects take hours to appear and last longer

Second messengers and amplification

One activated receptor can activate many G proteins, and each enzyme they turn on makes many second-messenger molecules (cAMP, IP3, calcium). This amplification is one reason a small amount of drug can cause a large response and why spare receptors exist.

Tolerance, desensitisation and rebound

With continued exposure, receptors are phosphorylated and uncoupled from their G proteins (minutes), then internalised and degraded (hours to days). Beta-2 agonists and opioids show this clearly. Long-term blockade has the opposite effect: receptors increase, so abrupt withdrawal of an antagonist such as propranolol can leave the tissue over-sensitive (rebound tachycardia, angina).

Selectivity is relative

A drug that is selective for one receptor subtype at usual concentrations can act on others at higher concentrations. Selectivity reduces, but does not remove, side effects mediated by other receptors.

Test yourself

Think of the answer, then tap the question to see it.

Why do steroid hormones take hours to produce their effects?

They act on intracellular receptors that change gene transcription, so the response needs new proteins to be made.

What is meant by spare receptors?

A maximal response can occur when only part of the receptors are occupied, because the signal is amplified downstream.

Why can stopping a beta blocker suddenly cause rebound tachycardia?

Long-term blockade increases the number or sensitivity of beta receptors; when the blocker is removed, normal catecholamines act on more receptors.

Which G protein raises cAMP and which lowers it?

Gs stimulates adenylyl cyclase and raises cAMP; Gi inhibits it and lowers cAMP.

Add to my cards (4)

Example drugs

← All of pharmacology

Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: 9.1 Signaling Molecules and Cellular Receptors (OpenStax (Rice University), 2018); 15.1 Divisions of the Autonomic Nervous System (OpenStax (Rice University), 2022); 15.4 Drugs that Affect the Autonomic System (OpenStax (Rice University), 2022).

Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake

Representative model, for educational purposes only.