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Hormonal Control:
ADH & Aldosterone

Discover how antidiuretic hormone and aldosterone work together to regulate water balance, blood pressure, and electrolyte concentration in the human body.

Anatomy & Physiology

Why Water Balance Matters

Your body is roughly 60% water by mass. Every cell depends on a precise ratio of water to solutes. If this ratio shifts even slightly, cells can swell, shrink, or lose the ability to carry out essential chemical reactions.

Meet the Two Hormones

ADH (Vasopressin)
Produced by the hypothalamus, stored and released by the posterior pituitary. Controls water reabsorption in the collecting ducts of the nephron.
Aldosterone
Produced by the adrenal cortex (zona glomerulosa). Controls \(\text{Na}^+\) reabsorption and \(\text{K}^+\) secretion in the distal convoluted tubule and collecting duct.

The Nephron: Where It All Happens

Glomerulus Bowman's Capsule PCT Loop of Henle DCT Aldosterone acts here Collecting Duct ADH acts here To ureter

How ADH Works

1
Stimulus: Osmoreceptors in the hypothalamus detect a rise in blood osmolarity (above ~300 mOsm/L).
2
Release: The posterior pituitary secretes ADH into the bloodstream.
3
Target: ADH binds to receptors on collecting duct cells, triggering insertion of aquaporin-2 channels.
4
Effect: Water is reabsorbed from the filtrate back into the blood. Urine becomes more concentrated and lower in volume.

ADH Negative Feedback Loop

Blood osmolarity rises Hypothalamus detects Posterior pituitary releases ADH Collecting duct reabsorbs water Blood osmolarity decreases Negative Feedback

How Aldosterone Works

1
Stimulus: Blood pressure drops or blood \(\text{Na}^+\) falls. The juxtaglomerular cells of the kidney release renin.
2
Cascade: Renin converts angiotensinogen to angiotensin I, which ACE converts to angiotensin II.
3
Release: Angiotensin II stimulates the adrenal cortex to secrete aldosterone.
4
Effect: Aldosterone increases \(\text{Na}^+\)/water reabsorption and \(\text{K}^+\) secretion in the DCT. Blood volume and pressure rise.

The RAAS Pathway

Low blood pressure / Low \(\text{Na}^+\)
 Kidney releases Renin Angiotensinogen → Angiotensin I ACE → Angiotensin II Aldosterone released
\(\text{Na}^+\) / \(\text{H}_2\text{O}\) reabsorbed → BP rises
 Negative Feedback Also causes vasoconstriction

ADH vs. Aldosterone: Key Distinctions

ADH Aldosterone
Source Posterior pituitary Adrenal cortex
Stimulus High blood osmolarity Low blood pressure / low \(\text{Na}^+\)
Primary target Collecting duct DCT & collecting duct
What it reabsorbs Water only \(\text{Na}^+\) (water follows)
Mechanism Aquaporin-2 insertion \(\text{Na}^+/\text{K}^+\) pump upregulation
Net effect on urine Concentrated, low volume Less \(\text{Na}^+\), more \(\text{K}^+\)

How to Predict the Hormonal Response

1
Identify the stimulus. Is it a change in osmolarity (solute concentration) or blood pressure / volume?
2
Match the hormone. Osmolarity change → ADH. Blood pressure/volume change → Aldosterone (via RAAS).
3
Determine direction. High osmolarity → ADH increases. Low BP → Aldosterone increases. Reverse for opposite stimuli.
4
Trace the effect. More ADH → more water reabsorbed → dilute blood, concentrated urine. More aldosterone → more \(\text{Na}^+\)/water reabsorbed → higher BP.
5
Check for negative feedback. Once homeostasis is restored, hormone release stops.

Example 1: Dehydration

Scenario: A runner finishes a marathon on a hot day. She has lost significant water through sweat. Her blood osmolarity has increased.

Example 2: Hemorrhage

Scenario: A patient experiences significant blood loss from a wound. Blood volume and pressure drop sharply.

Example 3: Over-Hydration

Scenario: A student drinks 3 liters of water in one hour. Blood osmolarity drops significantly below the normal set point.

Working Together: Dual Response

Severe dehydration ADH increases Water reabsorbed Aldosterone increases
\(\text{Na}^+\) & water reabsorbed
 Blood volume rises Osmolarity normalizes

Clinical Connections

Diabetes Insipidus
Insufficient ADH production or kidney resistance to ADH. Results in massive output of dilute urine (up to 20 L/day) and extreme thirst.
Conn's Syndrome
Excess aldosterone from an adrenal tumor. Causes persistent \(\text{Na}^+\) retention, hypertension, and dangerously low \(\text{K}^+\) (hypokalemia).
Addison's Disease
Adrenal cortex underproduces aldosterone. Leads to \(\text{Na}^+\) loss, low blood pressure, dehydration, and hyperkalemia.

Common Mistakes

✕ Mixing up the sources
ADH comes from the posterior pituitary, NOT the adrenal glands. Aldosterone comes from the adrenal cortex, NOT the pituitary.
✕ "ADH reabsorbs sodium"
ADH reabsorbs water only. It is aldosterone that reabsorbs \(\text{Na}^+\). Water follows \(\text{Na}^+\) passively when aldosterone acts.
✕ Confusing the stimuli
ADH responds to osmolarity changes detected by osmoreceptors. Aldosterone responds to blood pressure/volume changes via RAAS.

Question 1 of 5

A patient's blood osmolarity is significantly elevated. Which hormone will be released in response?

Question 2 of 5

What is the primary action of aldosterone on the nephron?

Question 3 of 5

A student drinks an excessive amount of water. What happens to ADH levels and urine output?

Question 4 of 5

In the RAAS pathway, which enzyme converts angiotensinogen to angiotensin I?

Question 5 of 5

A patient with Conn's syndrome (excess aldosterone) would most likely present with which combination of symptoms?