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Which hormone is responsible for the reabsorption of water in the renal tubules and is secreted by the posterior pituitary?
Options
1
Aldosterone
2
ADH (Antidiuretic Hormone / Vasopressin)
3
Atrial Natriuretic Peptide
4
Renin
Correct Answer
ADH (Antidiuretic Hormone / Vasopressin)
Solution
1

Key clues: "water reabsorption in renal tubules" + "posterior pituitary"

A: Aldosterone = adrenal cortex (not posterior pituitary) ✗

B: ADH (Vasopressin) = synthesized in hypothalamus, released from posterior pituitary ✓

2

C: ANP = from cardiac atria, causes Na+/water LOSS ✗

D: Renin = from juxtaglomerular cells, enzyme not hormone ✗

Answer: ADH (Antidiuretic Hormone / Vasopressin)

ADH: hypothalamus (synthesis) → posterior pituitary (release)
Acts on collecting duct: inserts AQP2 → water reabsorption
Theory: Human Physiology
1. Kidney Structure and Function

Nephron: functional unit of kidney. ~1 million per kidney. Parts: Glomerulus (capillary tuft) + Bowman capsule = renal corpuscle. Proximal convoluted tubule (PCT). Loop of Henle (descending + ascending limbs). Distal convoluted tubule (DCT). Collecting duct (CD). Filtration: glomerular filtration rate (GFR) = 125 mL/min = 180 L/day. Filtration pressure: hydrostatic pressure - oncotic pressure - capsule pressure. Ultrafiltrate: plasma minus large proteins and cells. Reabsorption: PCT reabsorbs ~65-70% of filtrate. Glucose, amino acids (Tm-limited), Na+, Cl-, HCO3-, water. Loop of Henle: creates medullary osmotic gradient. Countercurrent multiplication. DCT and CD: fine-tuning of Na+, K+, water (under hormonal control: aldosterone, ADH, ANP). Secretion: organic acids, drugs, K+, H+ into tubular fluid.

2. ADH (Vasopressin) Mechanism

ADH = AVP (arginine vasopressin) in humans. 9 amino acid peptide. Synthesized in supraoptic nuclei (SON) and paraventricular nuclei (PVN) of hypothalamus. Transported along axons to posterior pituitary where stored in Herring bodies. Released into blood in response to: hypertonicity (most potent stimulus, detected by osmoreceptors in hypothalamus, threshold ~280 mOsm/kg), hypovolemia (detected by baroreceptors in carotid sinus, aortic arch), nausea, pain, stress, hypoglycaemia, nicotine, morphine, angiotensin II. Inhibited by: hypotonicity, hypervolemia, alcohol (blocks ADH release - major cause of dehydration/hangover). Mechanism at kidney: V2 receptor (collecting duct principal cells) → Gs → adenylyl cyclase → cAMP → PKA → phosphorylates AQP2 vesicles → exocytosis → AQP2 in apical membrane → water permeability increases → water reabsorbed into interstitium → osmolarity rises, urine volume falls.

3. RAAS - Renin-Angiotensin-Aldosterone System

RAAS: major blood pressure and volume regulator. Renin: enzyme, from juxtaglomerular (JG) cells of afferent arteriole. Released when: low blood pressure (decreased stretch of afferent arteriole), low Na+ delivery to macula densa (DCT cells detecting NaCl), sympathetic stimulation (beta-1 receptors). Renin cleaves: angiotensinogen (from liver) → angiotensin I (10 aa). ACE (angiotensin-converting enzyme): from lung endothelium. Cleaves angiotensin I (10 aa) → angiotensin II (8 aa). Angiotensin II effects: vasoconstriction (AT1 receptor on vascular smooth muscle) → increases BP. Stimulates aldosterone release from adrenal cortex → Na+ and water retention. Stimulates ADH release. Stimulates thirst. ACE inhibitors (lisinopril, enalapril): block ACE → less Ang II → lower BP → less aldosterone → Na+/water loss. ARBs (losartan, valsartan): block AT1 receptor. Both used in hypertension, heart failure, diabetic nephropathy.

4. Regulation of Na+ and K+ Balance

Aldosterone: from adrenal cortex zona glomerulosa. Stimulated by angiotensin II, high plasma K+ (direct effect on adrenal), low Na+, ACTH. Mechanism: mineralocorticoid receptor (MR) → nuclear receptor → gene transcription → increases: ENaC (epithelial Na+ channel) on apical membrane of principal cells, Na+/K+ ATPase on basolateral membrane. Effect: Na+ reabsorbed, K+ and H+ excreted. Water follows Na+ (no AQP required). Hyperaldosteronism (Conn syndrome): excess aldosterone → hypertension, hypokalaemia, metabolic alkalosis. Hypoaldosteronism (Addison disease): low aldosterone → hyperkalaemia, hyponatremia, low BP, metabolic acidosis. ANP (Atrial Natriuretic Peptide): from cardiac atria when atrial pressure increases. Opposes RAAS. Causes: natriuresis (Na+ excretion), diuresis, vasodilation, suppresses renin and aldosterone. BNP (brain natriuretic peptide): from ventricles in heart failure. Diagnostic marker for heart failure.

5. Glomerular Filtration

Filtration barrier: fenestrated endothelium + basement membrane (negatively charged) + podocytes with slit diaphragm. Slit diaphragm proteins: nephrin, podocin. Mutations → nephrotic syndrome. GFR = 125 mL/min = 7500 mL/hr = 180 L/day. Only 1.5 L excreted = 99% reabsorbed. Measurement: inulin clearance (gold standard, freely filtered, not reabsorbed or secreted). Clinical: eGFR from serum creatinine (MDRD or CKD-EPI formula). CKD staging: GFR > 90 (stage 1) to GFR < 15 (stage 5 = kidney failure). Filtration forces: Glomerular hydrostatic pressure (pushes out): ~60 mmHg. Oncotic pressure of plasma proteins (pulls in): ~32 mmHg. Bowman capsule pressure (opposes): ~18 mmHg. Net filtration pressure: 60 - 32 - 18 = +10 mmHg (outward). Afferent arteriole constriction (SNS, angiotensin II) decreases GFR. Efferent arteriole constriction (angiotensin II) increases GFR (initially).

6. Renal Acid-Base Regulation

Kidney regulates pH by: excreting H+ (generates new HCO3-) or excreting HCO3-. PCT: reabsorbs ~85% of filtered HCO3- (via NHE3: Na+/H+ antiporter; H+ + HCO3- → H2CO3 → CO2 + H2O, then CO2 re-enters cell → reformed HCO3- excreted basolaterally). DCT/CD: alpha-intercalated cells: H+-ATPase pumps H+ into lumen. H2PO4- buffer (titratable acid), NH3/NH4+ buffer (ammonium excretion). New HCO3- generated for each H+ excreted. Beta-intercalated cells: secrete HCO3-, reabsorb Cl- (in alkalosis). Acid-base disorders: Respiratory acidosis: CO2 rises → pH falls. Renal compensation: increases H+ secretion, HCO3- reabsorption. Metabolic acidosis: HCO3- falls → pH falls. Respiratory compensation: hyperventilation. Renal compensation: more H+ excretion. Henderson-Hasselbalch: pH = 6.1 + log([HCO3-]/0.0307 x pCO2).

7. Hormonal Control of Kidney Function

ADH: collecting duct water reabsorption (via AQP2). Aldosterone: DCT and CD Na+ reabsorption, K+/H+ excretion. ANP: opposes RAAS, promotes Na+ and water excretion. Parathyroid hormone (PTH): increases Ca2+ reabsorption in DCT (calcium-sensing receptor), decreases phosphate reabsorption (PCT), activates 25-hydroxyvitamin D3 to 1,25-dihydroxyvitamin D3 (calcitriol) in proximal tubule. Calcitriol: increases intestinal Ca2+ absorption, increases renal Ca2+ reabsorption. Essential for Ca2+ homeostasis. Erythropoietin (EPO): produced by peritubular cells when hypoxia detected. Stimulates RBC production in bone marrow. Recombinant EPO used for anaemia of CKD. Dopamine: low-dose promotes natriuresis. High-dose (vasopressor): vasoconstriction. Glucocorticoids: have mineralocorticoid activity (mild, but significant in cortisol excess/Cushing syndrome).

8. Renal Diseases

Acute kidney injury (AKI): rapid decline in GFR. Pre-renal: decreased blood flow (dehydration, heart failure, sepsis). Intrinsic: direct kidney damage (ischaemia, nephrotoxins: NSAIDs, aminoglycosides, contrast). Post-renal: obstruction (kidney stones, prostate). Chronic kidney disease (CKD): GFR < 60 mL/min/1.73m2 for >3 months. Causes: diabetes (most common, 40%), hypertension (second, 25%), glomerulonephritis. Complications: anaemia (low EPO), hypertension, acidosis, hyperkalaemia, bone disease (low calcitriol → secondary hyperparathyroidism). Treatment: CKD stage 5 = dialysis (haemodialysis or peritoneal dialysis) or renal transplant. Glomerulonephritis: inflammation of glomeruli. Nephrotic syndrome: heavy proteinuria (>3.5 g/day), hypoalbuminaemia, oedema. Nephritic syndrome: haematuria, hypertension, oliguria, mild proteinuria. Kidney stones (nephrolithiasis): calcium oxalate most common (80%). Uric acid stones (gout). Struvite (infection).

Frequently Asked Questions
1. What is the mechanism of action of ADH on collecting duct cells at the molecular level? ⌄
ADH binds V2 receptor (vasopressin receptor 2) on basolateral membrane of collecting duct principal cells. V2 is a GPCR coupled to Gs (stimulatory G protein). Signalling cascade: V2 → Gs → adenylyl cyclase activated → cAMP increases → PKA (protein kinase A) activated → PKA phosphorylates AQP2 (aquaporin-2, water channel protein) on Ser256 → Phospho-AQP2 vesicles traffic to apical membrane → exocytosis inserts AQP2 into apical membrane → water permeability dramatically increases → water flows from tubular lumen (dilute urine) down osmotic gradient to hypertonic medullary interstitium → blood. Short-term (minutes): insertion of pre-formed AQP2 vesicles. Long-term (hours to days): ADH also activates transcription factor CREB → AQP2 gene expression increases → more AQP2 protein made. Nephrogenic diabetes insipidus: mutations in V2 receptor or AQP2 gene → kidney unresponsive to ADH → dilute urine despite high ADH levels.
2. Compare ADH and aldosterone in terms of water and salt reabsorption? ⌄
ADH (vasopressin): site = collecting duct, stimulus = high plasma osmolarity / low blood volume, mechanism = V2 receptor → cAMP → PKA → AQP2 insertion, effect = water reabsorption ONLY (not Na+), urine becomes concentrated (high osmolarity, low volume), regulates osmolarity primarily. Aldosterone: site = DCT and collecting duct, stimulus = angiotensin II, high K+, low Na+, mechanism = mineralocorticoid receptor (nuclear receptor) → gene transcription → ENaC + Na+/K+ATPase upregulation, effect = Na+ reabsorption + K+ excretion (water follows Na+ osmotically but INDIRECTLY), regulates volume and Na+/K+ balance primarily. Key distinction: ADH = pure water reabsorption (no Na+ movement). Aldosterone = Na+ reabsorption (water follows passively). In dehydration: both ADH and aldosterone are released. ADH concentrates urine. Aldosterone retains Na+ and water to restore blood volume. Together they restore both osmolarity and volume.
3. What is diabetes insipidus and how is it different from diabetes mellitus? ⌄
Diabetes insipidus (DI): inability to produce or respond to ADH → large volumes of dilute urine (polyuria, 3-20 L/day) + compensatory polydipsia. Central DI: inadequate ADH production from hypothalamus/posterior pituitary. Causes: head trauma, tumour (craniopharyngioma), infection, autoimmune, idiopathic. Treatment: desmopressin (synthetic ADH analogue). Nephrogenic DI: kidneys unresponsive to ADH. Causes: inherited (V2R mutation, AQP2 mutation), lithium toxicity, hypercalcaemia, hypokalaemia. Treatment: thiazide diuretics (paradoxically reduce urine volume by causing mild hypovolemia, activating Na+/water retention), NSAIDs. Diabetes mellitus (DM): inability to regulate blood glucose. Type 1: autoimmune destruction of beta cells → no insulin. Type 2: insulin resistance + progressive beta cell dysfunction. Cause of polyuria in DM: hyperglycaemia → glucose in filtrate exceeds Tm (tubular maximum ~180 mg/dL) → glucose not fully reabsorbed → osmotic diuresis → takes water with it. Both cause polyuria/polydipsia but mechanisms entirely different. The shared name "diabetes" (Greek: siphon, to pass through) reflects the polyuria.
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