Physiology · Renal, fluids and acid–base
Sodium and extracellular volume regulation (with natriuretic peptides) !
- Regulation
- Exam priority: high
The body's total sodium decides how much fluid sits outside the cells. The kidney adjusts it with hormones that keep or shed salt.
Updated 2026-11-01
Also called: Effective circulating volume, Atrial natriuretic peptide, Pressure natriuresis
See it in 3D: Kidneys · Right atrium · Left adrenal gland · Carotid bifurcation
What it is
Total body sodium sets extracellular volume, because water follows it through ADH and thirst. The body does not measure sodium directly: it senses effective circulating volume with pressure and stretch sensors. When volume falls, the renin–angiotensin–aldosterone system and the sympathetic system retain Na⁺; when it rises, natriuretic peptides and pressure natriuresis remove it.
How it works, step by step
- Effective circulating volume falls (bleeding, vomiting, diarrhea) and pressure drops in arteries and atria.
- Baroreceptors activate the sympathetic system, which constricts vessels and stimulates renin through β1 receptors.
- Lower afferent arteriole perfusion and less NaCl at the macula densa also release renin.
- Angiotensin II constricts the efferent, stimulates proximal NHE3 and releases aldosterone, ADH and thirst.
- Aldosterone increases ENaC in the collecting duct: Na⁺ is retained, and water with it.
- As volume recovers, the atria stretch, ANP is released, renin falls and the kidney excretes sodium again.
- Over the long term, high arterial pressure increases Na⁺ excretion (pressure natriuresis) until balance returns.
Hormone axes and feedback
Renin–angiotensin–aldosterone systemLesion None (normal)
Tap a box to see the hormone, or choose a lesion to see the lab pattern.
- Stimulates (+)
- Inhibits / negative feedback (−)
- Level ↑
- Level ↓
Reference values
| Parameter | Value | Note |
|---|---|---|
| Plasma sodium | 135–145 mEq/L | |
| Extracellular water | ≈ 1/3 of body water | ≈ 14 L in 70 kg |
| Na⁺ filtered per day | ≈ 25,000 mEq | < 1% excreted |
| FENa when sodium is retained | < 1% | without diuretics |
Approximate values for a healthy adult at rest; each laboratory sets its own ranges.
Regulation
- +Angiotensin II: Retains Na⁺ in the proximal tubule, releases aldosterone and ADH.
- +Aldosterone: Retains Na⁺ (ENaC) in the collecting duct in exchange for K⁺ and H⁺.
- +Renal sympathetic nerves: Release renin, constrict the afferent and increase tubular reabsorption.
- −ANP and BNP: Dilate the afferent, raise GFR, inhibit renin, aldosterone and collecting duct reabsorption.
- −Pressure natriuresis: High arterial pressure → less reabsorption → more Na⁺ in urine.
- −Renal dopamine and prostaglandins: Promote local natriuresis.
Volume states
| State | Total sodium | Effective volume | Renal response | Example |
|---|---|---|---|---|
| Hypovolemia | ↓ | ↓ | Retains Na⁺ (FENa < 1%) | Gastroenteritis, bleeding |
| Edema with low effective volume | ↑ | ↓ | Keeps retaining Na⁺ | Heart failure, cirrhosis |
| True expansion | ↑ | ↑ | Excretes Na⁺ (ANP) | Aldosterone excess, kidney disease |
| SIADH | ≈ | ≈ or slightly ↑ | Excretes Na⁺ | Lung tumour, drugs |
Clinical notes
- In heart failure, low output activates RAAS and the sympathetic system; Na⁺ and water retention worsen congestion. That is why ACE inhibitors, ARBs and aldosterone antagonists help.
- In cirrhosis, splanchnic vasodilation lowers effective volume: ascites with very low urine sodium.
- Aldosterone excess causes hypertension with little edema: natriuretic 'escape' (ANP, pressure natriuresis) limits expansion.
Test yourself
Think of the answer, then tap the question to see it.
Why does a patient with heart failure and edema keep retaining sodium?
Total volume is high, but the output and pressure sensed by baroreceptors and the kidney are low: effective volume is low, so RAAS and the sympathetic system stay active.
What does atrial natriuretic peptide do to lower volume?
Released when the atria stretch, it dilates the afferent (raising GFR), inhibits renin and aldosterone and reduces Na⁺ reabsorption in the medullary collecting duct.
Why does primary hyperaldosteronism cause hypertension but rarely edema?
After some Na⁺ retention, expansion raises pressure and ANP: pressure natriuresis 'escapes' aldosterone's sodium effect, although K⁺ loss continues.
What does a FENa below 1% mean in an oliguric patient?
The tubules work and avidly reabsorb sodium because the kidney senses a low effective volume (a prerenal cause), if no diuretics were given.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- The renin–angiotensin–aldosterone system
- Long-term blood pressure control by the kidney
- ADH, thirst and water balance
- The baroreceptor reflex
- Distal tubule and collecting duct
- Dehydration and fluid overload
- Body fluid compartments
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: 25.9 Regulation of Fluid Volume and Composition (OpenStax (Rice University), 2022); 26.3 Electrolyte Balance (OpenStax (Rice University), 2022); Heart Failure (Congestive Heart Failure) (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 30). 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.