Physiology · Cell and membrane
Primary and secondary active transport !
- Mechanism
- Exam priority: medium
Cells spend energy to move substances against their gradient, using ATP pumps or riding on the sodium gradient.
Updated 2026-11-01
Also called: Sodium–potassium pump, Cotransport and exchange
What it is
Active transport moves solutes against their electrochemical gradient. In primary active transport the protein is an ATPase that uses ATP directly (Na⁺/K⁺-ATPase, H⁺/K⁺-ATPase, Ca²⁺-ATPase). In secondary active transport the carrier never touches ATP: it couples Na⁺ moving down its gradient to the uphill movement of another substance, either the same way (cotransport) or the opposite way (countertransport). In this way the Na⁺/K⁺-ATPase indirectly powers glucose absorption, renal ion handling and Ca²⁺ removal from the heart.
How it works, step by step
- The Na⁺/K⁺-ATPase binds 3 Na⁺ on the inside and is phosphorylated by ATP.
- It changes shape, releases the 3 Na⁺ outside and binds 2 K⁺ from the outside.
- Dephosphorylation returns it to its first shape, releasing the 2 K⁺ inside.
- This keeps intracellular Na⁺ low: Na⁺ has a strong drive to enter down its gradient.
- Secondary carriers use that Na⁺ entry to drag glucose, amino acids or Cl⁻ against their gradients, or to push out H⁺ and Ca²⁺.
Active transporters that get asked
| Transporter | Type | Where | Relevance |
|---|---|---|---|
| Na⁺/K⁺-ATPase | Primary | Nearly all cells (basolateral in epithelia) | Target of digitalis; basis of the gradients |
| H⁺/K⁺-ATPase | Primary | Gastric parietal cell; collecting duct | Target of proton pump inhibitors |
| Ca²⁺-ATPase (SERCA, PMCA) | Primary | Sarcoplasmic reticulum; plasma membrane | Muscle relaxation; low cytosolic Ca²⁺ |
| SGLT1 / SGLT2 | Secondary (cotransport) | Intestine / proximal tubule | Oral rehydration; glycosuria |
| NKCC2 / NCC | Secondary (cotransport) | Loop of Henle / distal tubule | Targets of loop and thiazide diuretics |
| Na⁺/Ca²⁺ exchanger (NCX) | Secondary (countertransport) | Cardiac myocyte | Mediates digoxin's inotropic effect |
Clinical notes
- Oral rehydration: SGLT1 absorbs glucose together with Na⁺ and water follows, even in cholera; that is why rehydration salts save lives in childhood diarrhoea.
- Digitalis toxicity: nausea, visual changes and arrhythmias; hypokalaemia and kidney failure promote it.
- Therapeutic glycosuria: SGLT2 inhibitors block proximal glucose reabsorption and increase its urinary loss.
Test yourself
Think of the answer, then tap the question to see it.
Why does digoxin increase the heart's force of contraction?
By inhibiting the Na⁺/K⁺-ATPase it raises intracellular Na⁺; the gradient the NCX uses to remove Ca²⁺ shrinks, Ca²⁺ builds up in the reticulum and each beat releases more.
Why do oral rehydration salts contain glucose and not just salt?
Glucose drives SGLT1 cotransport with Na⁺, which keeps working in secretory diarrhoea; the absorbed Na⁺ pulls water with it.
Why is a patient with hypokalaemia more sensitive to digoxin?
K⁺ and digoxin compete for the same site on the Na⁺/K⁺-ATPase; with little K⁺, more digoxin binds and its effect and toxicity rise.
If the Na⁺/K⁺-ATPase stops, what happens to glucose uptake by SGLT?
It falls: intracellular Na⁺ rises, the gradient driving SGLT is lost and glucose is no longer concentrated in the cell.
Related topics
- Membrane transport: diffusion, channels and carriers
- Glucose transport maximum and renal threshold
- Proximal tubule transport
- Gastric acid secretion
- Carbohydrate digestion and absorption
- Transport in the loop of Henle
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: 3.1 The Cell Membrane (OpenStax (Rice University), 2022); 26.3 Electrolyte Balance (OpenStax (Rice University), 2022); Dehydration: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 4). 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.