Vasopressin (Antidiuretic Hormone)
Origin: Posterior pituitary
Location of Action: Collecting duct, apical cell membrane
Function: Directs the addition of aquaporins (AQP2) in the apical
membrane, leading to the absorption of water.
Mechanism of Action:
1. Increases the insertion of aquaporin-2 channels in the collecting
ducts, enhancing water reabsorption into the bloodstream.
2. Reduces urine output and concentrates urine.
3. Negative feedback: Water reabsorption dilutes plasma,
reducing ADH secretion.
Stimuli:
1. HIGH PLASMA OSMOLARITY: detected by
stretch-sensitive hypothalamic osmoreceptors
(DIRECT)
a. When osmolarity increases (>280mOsM),
neurons shrink, stop firing, indicating need to
CVCC for absorption (preservation) of water,
release of vasopressin increases.
2. LOW BLOOD VOLUME: detected by atrial stretch
receptors
a. When blood volume decreases, neurons stop
firing, indicating need to CVCC for absorption of
water, release of vasopressin increases
3. LOW BLOOD PRESSURE: detected by aortic and
carotid baroreceptors in the atria
a. When blood pressure decreases, neurons stop
firing, indicating need to CVCC for absorption of
water, release of vasopressin increases
4. CIRCADIAN RHYTHM: increased vasopressin
released at night. (DIRECT)
, Aldosterone
Origin: Adrenal Cortex (zona glomerulosa)
Location of Action: Distal tubule and collecting duct Principal Cells, apical cell membrane
Function: Directs the addition of ENaC and in the apical membrane and Na+-K+-ATPase in the basolateral
membrane, leading to the absorption of Na+ and excretion of K+.
Mechanism of Action:
1. Increases sodium reabsorption and potassium excretion by upregulating sodium-potassium pumps
and epithelial sodium channels (ENaCs).
2. Water often follows sodium osmotically (ONLY if ADH is also present), indirectly increasing blood
volume.
3. Negative feedback via normalization of blood pressure and potassium levels.
Stimulus for Release:
1. LOW BLOOD PRESSURE: Via the
renin-angiotensin-aldosterone system, specifically
angiotensin II.
Macula densa cells sensing less Na+ flow, trigger renin
release by JGA cells → … → ALD
Increased sympathetic input triggered by the CVCC in
response to low BP or low BV (baroreceptors) leads to
increased renin production → .. → ALD
2. HIGH [K+]: High serum potassium (direct stimulus).
Serum potassium concentrations are the most potent
stimulator of aldosterone secretion.
3. ACTH (minor role)
Stress stimulates the release of ACTH.
Origin: Posterior pituitary
Location of Action: Collecting duct, apical cell membrane
Function: Directs the addition of aquaporins (AQP2) in the apical
membrane, leading to the absorption of water.
Mechanism of Action:
1. Increases the insertion of aquaporin-2 channels in the collecting
ducts, enhancing water reabsorption into the bloodstream.
2. Reduces urine output and concentrates urine.
3. Negative feedback: Water reabsorption dilutes plasma,
reducing ADH secretion.
Stimuli:
1. HIGH PLASMA OSMOLARITY: detected by
stretch-sensitive hypothalamic osmoreceptors
(DIRECT)
a. When osmolarity increases (>280mOsM),
neurons shrink, stop firing, indicating need to
CVCC for absorption (preservation) of water,
release of vasopressin increases.
2. LOW BLOOD VOLUME: detected by atrial stretch
receptors
a. When blood volume decreases, neurons stop
firing, indicating need to CVCC for absorption of
water, release of vasopressin increases
3. LOW BLOOD PRESSURE: detected by aortic and
carotid baroreceptors in the atria
a. When blood pressure decreases, neurons stop
firing, indicating need to CVCC for absorption of
water, release of vasopressin increases
4. CIRCADIAN RHYTHM: increased vasopressin
released at night. (DIRECT)
, Aldosterone
Origin: Adrenal Cortex (zona glomerulosa)
Location of Action: Distal tubule and collecting duct Principal Cells, apical cell membrane
Function: Directs the addition of ENaC and in the apical membrane and Na+-K+-ATPase in the basolateral
membrane, leading to the absorption of Na+ and excretion of K+.
Mechanism of Action:
1. Increases sodium reabsorption and potassium excretion by upregulating sodium-potassium pumps
and epithelial sodium channels (ENaCs).
2. Water often follows sodium osmotically (ONLY if ADH is also present), indirectly increasing blood
volume.
3. Negative feedback via normalization of blood pressure and potassium levels.
Stimulus for Release:
1. LOW BLOOD PRESSURE: Via the
renin-angiotensin-aldosterone system, specifically
angiotensin II.
Macula densa cells sensing less Na+ flow, trigger renin
release by JGA cells → … → ALD
Increased sympathetic input triggered by the CVCC in
response to low BP or low BV (baroreceptors) leads to
increased renin production → .. → ALD
2. HIGH [K+]: High serum potassium (direct stimulus).
Serum potassium concentrations are the most potent
stimulator of aldosterone secretion.
3. ACTH (minor role)
Stress stimulates the release of ACTH.
