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

# The resting membrane potential

- Mechanism
- Exam priority: high

The inside of a resting cell is negative compared with the outside, mainly because potassium leaks out through its channels.

Updated 2026-11-01

Also called: Resting potential

## Key points

- The resting potential lies near the K⁺ equilibrium potential (≈ −94 mV) because resting K⁺ permeability is far higher than Na⁺ permeability.
- Neuron ≈ −70 mV; skeletal muscle and ventricular myocyte ≈ −85 to −90 mV.
- The Na⁺/K⁺-ATPase (3 Na⁺ out / 2 K⁺ in) contributes only about −4 mV directly; its real job is keeping the gradients.
- Hyperkalaemia depolarises: first more excitable, then Na⁺ channels inactivate and the cell becomes less excitable (weakness, arrhythmias).
- Hypokalaemia hyperpolarises the membrane and changes cardiac repolarisation (U waves, arrhythmias).

## What it is

At rest, the inside of excitable cells sits between −70 and −90 mV relative to the outside. The main cause is K⁺: the resting membrane is very permeable to it, and as it leaves down its gradient it leaves negative charge behind. The Na⁺/K⁺-ATPase directly makes very little of the voltage, but it maintains the gradients that make it possible. Any change in extracellular K⁺ shifts the resting potential and changes excitability, above all in the heart.

## How it works, step by step

- The Na⁺/K⁺-ATPase builds up K⁺ inside (≈140 mEq/L) and keeps Na⁺ outside (≈142 mEq/L).
- At rest, K⁺ leak channels are open; K⁺ leaves down its chemical gradient.
- Each K⁺ that leaves strands an anion inside (proteins, phosphates) that cannot follow: the interior turns negative.
- The internal negativity holds K⁺ back; an equilibrium near −94 mV is reached.
- A small Na⁺ leak inwards shifts the voltage a few millivolts positive (≈ −86 mV).
- The pump, moving out more positive charge than it brings in, adds about −4 mV: rest settles near −90 mV.

### Action potential

**Rest** −70 mV **Threshold** −55 mV **Peak** +35 mV **Duration** ≈ 1–2 ms

Tap a phase (the pills above or its band) or a refractory period (ARP, RRP) at the base of the plot.

- Mainly Na⁺
- Mainly K⁺
- Rest
- Threshold
- ARP: absolute refractory period
- RRP: relative refractory period

Tap each phase of the neuron action potential; the trace starts and ends at the resting potential.

## Equations

**K⁺ equilibrium potential (Nernst, 37 °C)**EK = 61.5 × log([K+]o / [K+]i) ≈ 61.5 × log(4/140) ≈ −94 mV

**o**
extracellular

**i**
intracellular

See the Nernst and Goldman page for the multi-ion calculation.

## Typical values

| Parameter | Value | Note |
| --- | --- | --- |
| Neuron | ≈ −70 mV | |
| Skeletal muscle | ≈ −85 to −90 mV | |
| Ventricular myocyte | ≈ −85 to −90 mV | |
| Sinoatrial node | ≈ −55 to −60 mV | no stable rest |
| Normal serum K⁺ | ≈3.5–5.0 mEq/L | |

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

## What shifts the resting potential

| Change | Effect on rest | Excitability | Classic sign |
| --- | --- | --- | --- |
| [High extracellular K⁺](https://durgical.com/en/conditions/hyperkalaemia/) | Less negative (depolarises) | Rises first; then falls as Na⁺ channels inactivate | Peaked T waves, weakness |
| [Low extracellular K⁺](https://durgical.com/en/conditions/hypokalaemia/) | More negative (hyperpolarises) | Muscle less excitable; heart with altered repolarisation | U wave, cramps, ileus |
| Na⁺/K⁺-ATPase blocked | Slow depolarisation as gradients run down | Altered | Digitalis toxicity |
| [Low extracellular Ca²⁺](https://durgical.com/en/conditions/hypocalcaemia/) | Little change | Rises: Na⁺ channel threshold falls | Tetany, Chvostek sign |

## Clinical notes

- Hyperkalaemia in chronic kidney disease or crush injury: the main danger is arrhythmia; calcium gluconate stabilises the cardiac membrane without lowering K⁺.
- Hypokalaemia from diarrhoea or diuretics: muscle weakness, ileus and arrhythmias; it promotes digitalis toxicity.
- Periodic paralyses: channelopathies in which K⁺ shifts between compartments change the resting potential and cause episodic weakness.

## Memory aid

Potassium leaves, the house turns negative: K⁺ leak strands anions inside and the interior goes negative.

## Test yourself

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

## Why is the resting potential closer to the K⁺ equilibrium potential than to the Na⁺ one?

At rest the membrane is far more permeable to K⁺ (leak channels open). The voltage approaches the equilibrium of the most permeant ion.

## If the Na⁺/K⁺-ATPase is blocked, does the resting potential vanish at once?

No. It loses only about −4 mV at first; it then depolarises slowly as the Na⁺ and K⁺ gradients the pump maintained run down.

## Why does severe hyperkalaemia cause weakness rather than hyperexcitability?

Sustained depolarisation keeps many Na⁺ channels inactivated; without them normal action potentials cannot fire, so excitability falls.

## Why does hypocalcaemia cause tetany if it barely changes the resting potential?

Extracellular Ca²⁺ stabilises Na⁺ channels; without it they open with less depolarisation. Threshold falls and spontaneous firing appears.

## What is special about the 'rest' of the sinoatrial node?

It is not stable: it sits near −60 mV and depolarises on its own (funny and Ca²⁺ currents) to threshold, which gives it automaticity.

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## Related topics

- [The Nernst and Goldman equations](https://durgical.com/en/physiology/the-nernst-and-goldman-equations/)
- [The nerve action potential](https://durgical.com/en/physiology/the-nerve-action-potential/)
- [Ion channels and gating](https://durgical.com/en/physiology/ion-channels-and-gating/)
- [The ECG in potassium and calcium disorders](https://durgical.com/en/physiology/the-ecg-in-potassium-and-calcium-disorders/)
- [Potassium balance](https://durgical.com/en/physiology/potassium-balance/)
- [Refractory periods and excitability](https://durgical.com/en/physiology/refractory-periods-and-excitability/)

## Related conditions

- [Hyperkalaemia](https://durgical.com/en/conditions/hyperkalaemia/)
- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)
- [Hypocalcaemia](https://durgical.com/en/conditions/hypocalcaemia/)

## In Biochemistry

- [Na⁺/K⁺-ATPase (sodium pump)](https://durgical.com/en/biochemistry/enzymes/na-k-atpase/)

## In Pharmacology

- [Cardiac glycosides](https://durgical.com/en/pharmacology/classes/cardiac-glycosides/)

[← 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: [12.4 The Action Potential](https://openstax.org/books/anatomy-and-physiology-2e/pages/12-4-the-action-potential) (OpenStax (Rice University), 2022); [High potassium level: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/001179.htm) (MedlinePlus, US National Library of Medicine, 2026); [Low blood potassium: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000479.htm) (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 5). 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.

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