Cell signaling for physiology !

Concept
Exam priority: medium

Hormones and neurotransmitters bind receptors that switch on chains of signals inside the cell.

Updated 2026-11-01

Also called: Second messengers, Membrane and nuclear receptors

What it is

A chemical signal acts only on cells that carry its receptor. Water-soluble molecules (peptides, catecholamines) cannot cross the membrane: they bind surface receptors that activate G proteins, enzymes or channels, and second messengers amplify the signal. Lipid-soluble ones (steroids, thyroid hormone, vitamin D) enter the cell and activate nuclear receptors that change gene transcription. Knowing each hormone's pathway lets you predict its speed, duration and which drugs or toxins alter it.

How it works, step by step

The ligand (first messenger) binds its specific receptor.
The receptor changes shape and activates a transducer: a G protein, its own kinase activity or an associated JAK.
The transducer switches an enzyme on or off that makes a second messenger (cAMP, IP₃, DAG, Ca²⁺, cGMP).
The second messenger activates kinases (PKA, PKC, PKG) that phosphorylate effector proteins: channels, enzymes, transcription factors.
Each step multiplies the signal (amplification); phosphodiesterases and phosphatases switch it off.

Signalling pathways and examples

Pathway	Receptor	Messenger	Examples
Gs	G protein-coupled	↑cAMP → PKA	β1, β2, glucagon, TSH, ADH at V2
Gi	G protein-coupled	↓cAMP	α2, M2, opioids
Gq	G protein-coupled	IP₃ → Ca²⁺; DAG → PKC	α1, M3, angiotensin II (AT1), ADH at V1
cGMP	Guanylyl cyclase (soluble or membrane)	cGMP → PKG	Nitric oxide, atrial natriuretic peptide
Tyrosine kinase	Receptor with kinase activity	PI3K and MAPK cascades	Insulin, IGF-1, EGF
JAK-STAT	Receptor without its own kinase	JAK phosphorylates STAT	GH, prolactin, erythropoietin
Nuclear	Intracellular	Gene transcription	Cortisol, aldosterone, T₃, vitamin D

Clinical notes

Cholera: the toxin locks the enterocyte's Gs on; high cAMP opens the CFTR channel and causes massive watery diarrhoea.
Whooping cough: the toxin inactivates Gi; without the brake, cAMP rises in many cells.
Nephrogenic diabetes insipidus: the V2 receptor (Gs) fails; ADH cannot insert aquaporins and the urine stays dilute.

Test yourself

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

Why do cortisol's effects take hours while adrenaline's take seconds?

Cortisol acts through a nuclear receptor and needs gene transcription and protein synthesis; adrenaline uses a G protein and second messengers that modify proteins already present.

ADH acts on two different receptors. Which pathway does each use, and with what effect?

V2 (Gs, cAMP) in the collecting duct inserts aquaporins; V1 (Gq, IP₃/Ca²⁺) in vascular smooth muscle causes vasoconstriction.

Why does cholera toxin cause diarrhoea without destroying the epithelium?

It locks Gs in the active state; high cAMP holds CFTR open, Cl⁻ is secreted into the lumen and Na⁺ and water follow. The mucosa stays intact.

What do nitric oxide and atrial natriuretic peptide have in common?

Both raise cGMP (soluble or membrane guanylyl cyclase), activate PKG and relax vascular smooth muscle.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 17.2 Hormones (OpenStax (Rice University), 2022); 12.5 Communication Between Neurons (OpenStax (Rice University), 2022); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 75). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.