Part of the TeachMe Series

Active Transport

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Original Author(s): Charlotte Smith
Last updated: 8th April 2024
Revisions: 14

Original Author(s): Charlotte Smith
Last updated: 8th April 2024
Revisions: 14

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Cell membranes are selectively permeable. This means that they allow the movement of some molecules freely across them, but do not allow the free passage of others. In broad terms, there are three ways in which molecules move across membranes. These are the processes of diffusionosmosis and active transport. 

In this article, we will discuss active transport, and consider the clinical relevance of this.

Mechanism of Active Transport

Active transport is the movement of molecules from an area of lower concentration to a higher concentration, i.e. up a concentration gradient, via specialised membrane proteins.

As this is against the concentration gradient, it cannot occur passively. Therefore, active transport requires energy, which is provided by the breakdown of ATP. Active transport is a highly demanding metabolic process; some cells can use up to 50% of their energy on active transport alone.

A key example of an active transporter is the sodium-potassium (Na/KATP-ase) pump. This exports three sodium ions in return for two potassium ions. This is key to maintaining the resting membrane potential.


Some membrane proteins involved in facilitated diffusion or active transport can carry multiple molecules or ions at once – this is known as “co-transport”. Where the molecules move in the same direction, this is known as “symport”. Where some molecules move one way and others move the other, this is known as “anti-port”. The sodium-potassium pump is an example of an antiporter.

Fig 1 – Active transport proteins

Clinical Relevance – Drug Targets

The sodium/potassium ATPase pump is essential to many physiological processes, so targeting it with medication can be useful clinically. Conversely, drugs which act on the pump in addition to their main action can cause unwanted side effects. Examples of drugs affecting the Na/K ATPase include:

  • Spironolactone: An aldosterone antagonist, blocks the Na/K ATPase pump in the distal convoluted tubule and collecting duct. This reduces sodium reabsorption via the epithelial sodium channel (ENaC), and consequently reduces water reabsorption too. This is useful in heart failure and liver disease.
  • Digoxin: This blocks Na/K ATPase, mainly in the myocardium. This leads to an accumulation of intracellular calcium, which reduces heart rate by prolonging the cardiac action potential. It also increases the force of contraction of the myocardium. This is useful in heart failure and atrial fibrillation.
  • SteroidsGlucocorticoids have a degree of cross-reactivity at the mineralocorticoid receptor in the distal convoluted tubule/collecting duct. This increases the activity of Na/K ATPase, leading to the opposite effect of spironolactone. Over time, this leads to water retention and subsequently swelling (oedema) in these patients.