Resting membrane potential
Also known as: membrane potential, resting potential, Nernst equation, equilibrium potential, Goldman equation
The voltage across the plasma membrane of a resting cell (inside negative, typically −70 to −90 mV), generated mainly by K⁺ leaking out down the concentration gradient built by the Na⁺/K⁺-ATPase.
Overview
Two conditions create a membrane potential: an unequal ion distribution across the membrane and selective permeability. The Na⁺/K⁺-ATPase keeps K⁺ high inside (≈140 mM vs ≈4–5 mM outside) and Na⁺ high outside (≈145 mM vs ≈10–15 mM inside). At rest the membrane is far more permeable to K⁺ (through leak K⁺ channels) than to Na⁺. K⁺ diffuses out, leaving behind unbalanced negative charge (mostly on impermeant intracellular proteins and phosphates), until the inside-negative potential pulls on K⁺ as strongly as the concentration gradient pushes it out.
For each ion the equilibrium (Nernst) potential is the voltage at which electrical and chemical forces balance: E = (61.5/z) × log([ion]out/[ion]in) mV at 37 °C. Approximate values: E_K ≈ −90 to −95 mV, E_Na ≈ +60 to +65 mV, E_Ca ≈ +120 mV, E_Cl ≈ −70 to −80 mV (cell-dependent). The actual resting potential is a permeability-weighted average of these, given by the Goldman–Hodgkin–Katz equation; because K⁺ permeability dominates, Vm lies close to E_K but slightly less negative owing to a small Na⁺ leak. The pump itself contributes only a few millivolts directly (electrogenic).
Only a tiny number of ions need to move to establish the potential, so bulk concentrations hardly change. Excitable cells (neurons, muscle) use rapid, voltage-gated changes in permeability to generate action potentials; non-excitable cells use the potential to drive transport.
Function
- Basis of electrical excitability (action potentials, synaptic potentials).
- Driving force for electrogenic transport (e.g. Na⁺-coupled uptake).
- Regulates voltage-gated Ca²⁺ entry and secretion (e.g. insulin release from β cells).
- Physiology
Typical values: neurons ≈ −70 mV; skeletal and ventricular muscle ≈ −90 mV; smooth muscle ≈ −50 to −60 mV; erythrocytes ≈ −10 mV (Cl⁻-dominated). Changes are described as depolarisation (less negative), repolarisation and hyperpolarisation (more negative).
Clinical significance
Hyperkalaemia and hypokalaemia
Raised extracellular K⁺ makes E_K less negative and depolarises cells; persistent depolarisation inactivates Na⁺ channels → muscle weakness, peaked T waves, conduction block and ventricular fibrillation. Treat urgently with IV calcium (membrane stabilisation), insulin–glucose and β2 agonists (shift K⁺ into cells). Hypokalaemia hyperpolarises cells → weakness, ileus, U waves and arrhythmias.
Test yourself
The resting membrane potential of most cells lies closest to the equilibrium potential of which ion?
- Na⁺
- K⁺
- Ca²⁺
- Cl⁻
Answer: K⁺
At rest K⁺ leak channels dominate membrane permeability, so Vm (≈ −70 to −90 mV) is near E_K (≈ −90 mV). Hyperkalaemia therefore depolarises cells and can cause cardiac arrhythmias.
Compiled from standard anatomy and physiology references — see the Cells & Tissues sources. For education only; not medical advice.