Physiology · Cell and membrane
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
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 mVThreshold −55 mVPeak +35 mVDuration ≈ 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
Equations
- 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⁺ | Less negative (depolarises) | Rises first; then falls as Na⁺ channels inactivate | Peaked T waves, weakness |
| Low extracellular K⁺ | 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⁺ | 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.
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.
Related topics
- The Nernst and Goldman equations
- The nerve action potential
- Ion channels and gating
- The ECG in potassium and calcium disorders
- Potassium balance
- Refractory periods and excitability
Related conditions
In Biochemistry
In Pharmacology
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 (OpenStax (Rice University), 2022); High potassium level: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Low blood potassium: MedlinePlus Medical Encyclopedia (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.