Question
How do the kidneys regulate water and salt balance in the body? Explain the roles of ADH and aldosterone. What happens to urine concentration when you are dehydrated vs. when you drink excess water? How does the countercurrent mechanism help produce concentrated urine?
(NEET pattern — integrated mechanism)
Solution — Step by Step
| Hormone | Source | Trigger | Action on Kidney | Result |
|---|---|---|---|---|
| ADH (Antidiuretic Hormone / Vasopressin) | Posterior pituitary | High blood osmolarity (dehydration) | Makes collecting duct permeable to water → water reabsorbed | Concentrated urine, less volume |
| Aldosterone | Adrenal cortex (zona glomerulosa) | Low blood Na⁺, high K⁺, low blood pressure (via RAAS) | Increases Na⁺ reabsorption in DCT and collecting duct → water follows Na⁺ | Blood pressure rises, dilute urine |
| Condition | ADH Level | Collecting Duct | Urine |
|---|---|---|---|
| Dehydrated | High ADH | Very permeable → maximum water reabsorption | Small volume, dark, concentrated |
| Excess water | Low ADH | Impermeable → water passes through as urine | Large volume, pale, dilute |
This is why your urine is dark yellow in the morning (mild dehydration overnight) and pale after drinking lots of water.
The loop of Henle and vasa recta work together to create a concentration gradient in the kidney medulla:
- Descending limb of loop of Henle: permeable to water, impermeable to solutes → water leaves, filtrate becomes concentrated
- Ascending limb: impermeable to water, actively pumps out NaCl → filtrate becomes dilute, but medullary interstitium becomes concentrated
- Vasa recta (blood vessels): run parallel to the loop, maintaining the gradient by countercurrent exchange — they do not wash away the salt
This gradient (300 mOsm/L at cortex → 1200 mOsm/L at inner medulla) allows the collecting duct to concentrate urine when ADH is present.
When blood pressure drops:
- Juxtaglomerular cells in kidney release renin
- Renin converts angiotensinogen → angiotensin I
- ACE (in lungs) converts angiotensin I → angiotensin II
- Angiotensin II stimulates aldosterone release → Na⁺ reabsorption → blood pressure rises
graph TD
A["Blood Osmolarity High"] --> B["Hypothalamus detects"]
B --> C["Posterior Pituitary releases ADH"]
C --> D["Collecting Duct becomes permeable"]
D --> E["Water reabsorbed"]
E --> F["Concentrated urine, small volume"]
G["Blood Pressure Low"] --> H["Kidney releases Renin"]
H --> I["RAAS activates"]
I --> J["Aldosterone: Na+ reabsorbed"]
J --> K["Water follows Na+"]
K --> L["Blood pressure restored"]
style A fill:#fca5a5,stroke:#000
style F fill:#fbbf24,stroke:#000,stroke-width:2px
style G fill:#93c5fd,stroke:#000
Why This Works
Osmoregulation is a feedback system. Osmoreceptors in the hypothalamus detect blood concentration. When concentration rises (dehydration), ADH is released, causing the kidney to retain water. When concentration falls (excess water), ADH is suppressed, and water is excreted.
The countercurrent mechanism is the engineering marvel that makes this possible. Without the concentration gradient in the medulla, the collecting duct could not concentrate urine regardless of ADH levels. The loop of Henle creates the gradient; ADH controls how much the collecting duct uses it.
Common Mistake
Students confuse ADH and aldosterone. ADH primarily controls water reabsorption (makes collecting duct permeable to water). Aldosterone primarily controls sodium reabsorption (in DCT and collecting duct). Water follows sodium passively. Both result in increased blood volume, but the mechanisms and triggers are different. NEET tests this distinction directly.
For the countercurrent mechanism, remember: descending limb = “Drains water out” (permeable to water), ascending limb = “Actively pumps salt out” (impermeable to water). The net result: medulla becomes hypertonic (salty), which is what pulls water out of the collecting duct when ADH is present.