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[Physiology](https://durgical.com/en/physiology/) · [Cell and membrane](https://durgical.com/en/physiology/#s-cell)

# 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

## Key points

- Gs → adenylyl cyclase → ↑cAMP → PKA (β1, β2, D1, H2, V2, glucagon, TSH, ACTH, PTH, LH, FSH).
- Gi → ↓cAMP (α2, M2, D2, opioids). Gq → phospholipase C → IP₃ (releases Ca²⁺) and DAG (activates PKC) (α1, M1, M3, V1, AT1, GnRH, TRH).
- Receptor tyrosine kinase: insulin, IGF-1 and growth factors. JAK-STAT: GH, prolactin, EPO, cytokines.
- cGMP: nitric oxide (soluble guanylyl cyclase) and natriuretic peptide (membrane receptor) relax smooth muscle.
- Nuclear receptors (steroids, T₃, vitamin D, retinoids): slow effect through protein synthesis; lasts hours to days.

## 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.

## Memory aid

Gs adds, Gi subtracts, Gq calls the calcium: stimulates cAMP, inhibits it, or releases Ca²⁺ through IP₃.

## 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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## Related topics

- [Hormones: types, receptors and feedback](https://durgical.com/en/physiology/hormones-types-receptors-and-feedback/)
- [Adrenergic and cholinergic receptors](https://durgical.com/en/physiology/adrenergic-and-cholinergic-receptors/)
- [The main neurotransmitters](https://durgical.com/en/physiology/the-main-neurotransmitters/)
- [Islets and insulin: secretion and actions](https://durgical.com/en/physiology/islets-and-insulin-secretion-and-actions/)
- [Growth hormone and IGF-1](https://durgical.com/en/physiology/growth-hormone-and-igf-1/)

## In Biochemistry

- [G protein-coupled receptors and cAMP](https://durgical.com/en/biochemistry/topics/g-protein-coupled-receptors-and-camp/)
- [IP₃, DAG and calcium pathway](https://durgical.com/en/biochemistry/topics/ip-dag-and-calcium-pathway/)
- [Receptor tyrosine kinases](https://durgical.com/en/biochemistry/topics/receptor-tyrosine-kinases/)
- [Nuclear receptors](https://durgical.com/en/biochemistry/topics/nuclear-receptors/)
- [JAK–STAT pathway](https://durgical.com/en/biochemistry/topics/jak-stat-pathway/)
- [Hormone classes and mechanisms](https://durgical.com/en/biochemistry/topics/hormone-classes-and-mechanisms/)

[← All of physiology](https://durgical.com/en/physiology/)

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](https://openstax.org/books/anatomy-and-physiology-2e/pages/17-2-hormones) (OpenStax (Rice University), 2022); [12.5 Communication Between Neurons](https://openstax.org/books/anatomy-and-physiology-2e/pages/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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