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

# 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

## Key points

- Na⁺/K⁺-ATPase: 3 Na⁺ out and 2 K⁺ in per ATP; electrogenic and a large share of resting ATP use.
- Digoxin inhibits the Na⁺/K⁺-ATPase → intracellular Na⁺ rises → the Na⁺/Ca²⁺ exchanger removes less Ca²⁺ → more contractility.
- Hypokalaemia increases digoxin toxicity: both compete for the same site on the pump.
- Omeprazole irreversibly inhibits the parietal cell H⁺/K⁺-ATPase: the final step of acid secretion.
- Cotransport (SGLT1, NKCC2, NCC) and countertransport (Na⁺/H⁺, Na⁺/Ca²⁺) depend on the Na⁺ gradient.

## 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.

## Memory aid

The pump charges the battery; the cotransporters spend it: ATP builds the Na⁺ gradient and the others use it.

## 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.

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## Related topics

- [Membrane transport: diffusion, channels and carriers](https://durgical.com/en/physiology/membrane-transport-diffusion-channels-and-carriers/)
- [Glucose transport maximum and renal threshold](https://durgical.com/en/physiology/glucose-transport-maximum-and-renal-threshold/)
- [Proximal tubule transport](https://durgical.com/en/physiology/proximal-tubule-transport/)
- [Gastric acid secretion](https://durgical.com/en/physiology/gastric-acid-secretion/)
- [Carbohydrate digestion and absorption](https://durgical.com/en/physiology/carbohydrate-digestion-and-absorption/)
- [Transport in the loop of Henle](https://durgical.com/en/physiology/transport-in-the-loop-of-henle/)

## Related conditions

- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)

## In Biochemistry

- [Na⁺/K⁺-ATPase (sodium pump)](https://durgical.com/en/biochemistry/enzymes/na-k-atpase/)
- [H⁺/K⁺-ATPase (gastric proton pump)](https://durgical.com/en/biochemistry/enzymes/h-k-atpase/)
- [Membrane transport](https://durgical.com/en/biochemistry/topics/membrane-transport/)

## In Pharmacology

- [Digoxin](https://durgical.com/en/pharmacology/digoxin/)
- [Cardiac glycosides](https://durgical.com/en/pharmacology/classes/cardiac-glycosides/)
- [Omeprazole](https://durgical.com/en/pharmacology/omeprazole/)
- [Proton pump inhibitors (PPIs)](https://durgical.com/en/pharmacology/classes/proton-pump-inhibitors/)

[← 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: [3.1 The Cell Membrane](https://openstax.org/books/anatomy-and-physiology-2e/pages/3-1-the-cell-membrane) (OpenStax (Rice University), 2022); [26.3 Electrolyte Balance](https://openstax.org/books/anatomy-and-physiology-2e/pages/26-3-electrolyte-balance) (OpenStax (Rice University), 2022); [Dehydration: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000982.htm) (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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