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BiologyHuman Physiology
Statement I: Renin is a hormone secreted directly by the adrenal cortex.
Statement II: Juxtaglomerular cells in the kidney produce erythropoietin only.
Options
1
Both statements are correct
2
Statement I is correct but II is incorrect
3
Statement I is incorrect but II is correct
4
Both statements are incorrect
Correct Answer
Both statements are incorrect
Solution
1

Statement I: Renin secreted by adrenal cortex = FALSE

Renin is secreted by juxtaglomerular (JG) cells of afferent arteriole in kidney.

2

Statement II: JG cells produce erythropoietin only = FALSE

JG cells produce RENIN. Erythropoietin is produced by peritubular interstitial cells of kidney.

Answer: Both statements are incorrect

Renin = from JG cells of kidney (not adrenal cortex)
EPO = from peritubular cells of kidney (not JG cells)
Theory: Human Physiology
1. Juxtaglomerular Apparatus (JGA)

JGA: group of specialised cells near the glomerulus. Components: Juxtaglomerular (JG) cells: modified smooth muscle cells in afferent arteriole wall. Store and release renin. Macula densa: specialised DCT cells adjacent to JGA. Sense NaCl concentration in tubular fluid. Extraglomerular mesangial cells (Lacis cells): between arterioles and tubule. Signals for renin release: Low blood pressure (decreased stretch of afferent arteriole wall = baroreceptor mechanism). Low NaCl delivery to macula densa (tubuloglomerular feedback). Sympathetic stimulation (beta-1 adrenergic receptors on JG cells). Low angiotensin II (feedback). Prostaglandins (PGE2, PGI2) stimulate renin. Inhibited by: high blood pressure, high NaCl at macula densa, high angiotensin II (negative feedback). NSAIDs: inhibit prostaglandin synthesis → reduce renin release → reduce blood pressure (one mechanism of NSAID antihypertensive effect).

2. Erythropoietin (EPO)

EPO: glycoprotein hormone, MW ~34 kDa. Produced primarily by: peritubular interstitial cells (fibroblast-like cells) in the kidney cortex and outer medulla (~85%). Hepatocytes (~15%, increases in adults with kidney disease). Foetal liver: primary source of EPO before birth. Stimulus: tissue hypoxia (low O2). HIF-1alpha (hypoxia-inducible factor 1-alpha): transcription factor. Normally degraded by VHL protein under normoxia. Under hypoxia: HIF-1alpha accumulates → activates EPO gene transcription. VHL gene mutation: Chuvash polycythaemia, von Hippel-Lindau disease. EPO mechanism: binds EPO receptor (EpoR) on bone marrow erythroid progenitor cells → JAK2-STAT5 signalling → cell survival + proliferation + differentiation → increased RBC production. Time from EPO stimulus to new RBCs: ~5-7 days. Clinical: recombinant EPO (epoetin alfa): CKD anaemia, cancer-related anaemia. Misuse: blood doping in athletes.

3. Adrenal Gland Hormones

Adrenal cortex (steroid hormones from cholesterol): Zona glomerulosa (outermost): aldosterone. Stimulated by angiotensin II, high K+, ACTH (minor). Actions: principal cells of collecting duct → ENaC (Na+ channel) and Na+/K+ ATPase increase → Na+ reabsorption, K+ and H+ excretion. Zona fasciculata (middle): cortisol (glucocorticoid). Stimulated by ACTH. Multiple actions: glucose (increases gluconeogenesis, reduces insulin sensitivity), protein (catabolism), fat (redistribution to trunk/face), anti-inflammatory (reduces prostaglandins, cytokines), immunosuppressive, helps stress response. Zona reticularis (inner): androgens (DHEA, androstenedione). Minor contribution to sex steroid pool. Adrenal medulla (catecholamines): adrenaline/epinephrine (80%) and noradrenaline/norepinephrine (20%). Released in response to acute stress (fight-or-flight). Increases HR, BP, glucose, bronchodilation.

4. Kidney Hormones

Kidney as endocrine organ: (1) Renin: enzyme, not hormone strictly. From JG cells. Cleaves angiotensinogen → angiotensin I. (2) Erythropoietin (EPO): from peritubular interstitial cells. Stimulates erythropoiesis. (3) 1,25-dihydroxyvitamin D3 (calcitriol): 25-OH-D3 (from liver) hydroxylated at 1-alpha position by 1-alpha-hydroxylase in proximal tubule. Active form of vitamin D. Stimulated by PTH, hypophosphataemia. Inhibited by high FGF-23. Actions: increases intestinal Ca2+ and phosphate absorption, increases renal Ca2+ reabsorption, stimulates osteoclasts (bone resorption). (4) Prostaglandins: intrarenal. Dilate afferent arteriole, maintain GFR. (5) Kallikrein-kinin system: bradykinin (vasodilator) produced in kidney. NSAIDs: reduce renal prostaglandins → constrict afferent arteriole → reduce GFR → fluid retention → hypertension. Important side effect in patients with CKD or heart failure.

5. Blood Pressure Regulation

Short-term: baroreceptors (carotid sinus, aortic arch) → ANS → heart rate and peripheral vascular resistance. Adrenaline/noradrenaline. Long-term: RAAS (days-weeks): renin-angiotensin-aldosterone system. Na+ and water retention. Vasopressin (ADH): water retention. ANP: Na+/water excretion (opposes RAAS). Autoregulation: kidney maintains constant GFR despite blood pressure changes (myogenic reflex: increased pressure → afferent arteriole contracts). Normal BP: 120/80 mmHg. Hypertension: >130/80 mmHg. Primary (essential) hypertension: 95% of cases, no identifiable cause. Secondary hypertension: 5%, identifiable cause: renal disease (renovascular - renal artery stenosis increases renin; renal parenchymal), primary hyperaldosteronism (Conn syndrome), phaeochromocytoma (adrenaline/noradrenaline excess), Cushing syndrome (cortisol excess), thyroid disorders. Treatment of hypertension: lifestyle + drugs: ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, diuretics (thiazide = first-line).

6. Disorders of Adrenal Glands

Cushing syndrome: excess cortisol. Causes: pituitary adenoma (ACTH-secreting = Cushing disease, 65%), adrenal adenoma/carcinoma (15%), ectopic ACTH (small cell lung cancer, carcinoid, 20%), iatrogenic (exogenous glucocorticoids, most common). Features: central obesity (truncal fat + buffalo hump + moon face), thin skin (striae), muscle weakness (proximal myopathy), hypertension, diabetes/glucose intolerance, osteoporosis, psychiatric symptoms. Diagnosis: 24h urine cortisol, dexamethasone suppression test, midnight salivary cortisol. Addison disease: primary adrenal insufficiency. Destruction of adrenal cortex (autoimmune 70%, TB, metastases). Features: fatigue, weight loss, hyperpigmentation (elevated ACTH/MSH), hypotension, hyperkalaemia, hyponatremia, hypoglycaemia. Life-threatening adrenal crisis if acute. Treatment: hydrocortisone + fludrocortisone. Congenital adrenal hyperplasia (CAH): enzyme defects in cortisol synthesis. Most common: 21-hydroxylase deficiency → no cortisol → high ACTH → adrenal hyperplasia → excess androgens → ambiguous genitalia in females, precocious puberty in males.

7. Thyroid Hormones

Thyroid gland: follicular cells produce T3 (triiodothyronine) and T4 (thyroxine). Parafollicular C cells produce calcitonin. T4: prohormone. Deiodination in peripheral tissues (mainly liver and kidney) → T3 (active form). T3: binds nuclear thyroid hormone receptors (TRs, TR-alpha and TR-beta). Gene regulation. T3 effects: increase metabolic rate (stimulates Na+/K+ ATPase, mitochondriogenesis), positive inotropic and chronotropic effects on heart, growth and development (essential for brain development in first 3 years of life), bone maturation, thermogenesis. Regulation: hypothalamus → TRH (thyrotropin-releasing hormone) → anterior pituitary → TSH (thyroid-stimulating hormone) → thyroid → T3/T4. Negative feedback: T3/T4 inhibit TRH and TSH. Thyrotoxicosis: excess thyroid hormones. Tachycardia, weight loss, heat intolerance, diarrhoea, exophthalmos (in Graves disease). Graves disease: autoimmune, TSH receptor antibodies stimulate thyroid. Hypothyroidism: insufficient T3/T4. Fatigue, weight gain, cold intolerance, bradycardia, constipation, dry skin. Congenital hypothyroidism: cretinism (irreversible intellectual disability if untreated) - screened at birth.

8. Pituitary Gland

Anterior pituitary (adenohypophysis): GH (growth hormone): somatotrophs, stimulates IGF-1 from liver, growth. Excess in children: gigantism. Excess in adults: acromegaly (enlarged hands, feet, jaw). Deficiency: dwarfism. TSH (thyroid-stimulating hormone): thyrotrophs. ACTH: corticotrophs. FSH and LH: gonadotrophs. Prolactin: lactotrophs. Stimulates milk production. Excess: galactorrhoea, amenorrhoea, infertility. Posterior pituitary (neurohypophysis): stores and releases hormones made in hypothalamus. ADH/Vasopressin: from supraoptic nuclei (SON). Oxytocin: from paraventricular nuclei (PVN). Both transported along axons from hypothalamus to posterior pituitary. Oxytocin: stimulates uterine contractions during labour (positive feedback), milk ejection (let-down reflex). Also has social bonding roles. Synthetic: Pitocin used to induce labour. Pituitary tumours (pituitary adenomas): most common = prolactinoma (lactotroph adenoma). Treatment: dopamine agonists (cabergoline, bromocriptine) reduce prolactin and tumour size.

Frequently Asked Questions
1. What is the RAAS pathway and how does it regulate blood pressure? ⌄
Renin-Angiotensin-Aldosterone System: Start: Low blood pressure or low Na+ → JG cells release renin into blood. Step 1: Renin (enzyme) cleaves angiotensinogen (alpha-2 globulin from liver, ~57 kDa) → angiotensin I (decapeptide, 10 amino acids). Step 2: ACE (angiotensin-converting enzyme) on lung endothelium cleaves 2 C-terminal amino acids from Ang I → angiotensin II (octapeptide, 8 aa). ACE also degrades bradykinin (vasodilator) - side effect of ACE inhibitors: bradykinin accumulation → dry cough. Step 3: Angiotensin II actions via AT1 receptor: vasoconstriction (direct effect on vascular smooth muscle), stimulates aldosterone secretion from adrenal cortex zona glomerulosa, stimulates ADH release from posterior pituitary, stimulates thirst (hypothalamus), enhances Na+ reabsorption in PCT directly, stimulates SNS, cardiac hypertrophy (long-term). Net result: increased blood pressure and blood volume. Pharmacology: ACE inhibitors (lisinopril, enalapril) and ARBs (losartan, valsartan) block this system → lower BP. First-line for hypertension, heart failure, diabetic nephropathy, post-MI.
2. Distinguish between renin and aldosterone in terms of origin and function? ⌄
Renin: origin = juxtaglomerular (JG) cells of kidney (afferent arteriole). Chemical nature = enzyme (protein, aspartyl protease), NOT a steroid hormone. Function = cleaves angiotensinogen → angiotensin I. Is NOT a hormone itself (acts as an enzyme catalysing a reaction). Aldosterone: origin = zona glomerulosa of adrenal cortex. Chemical nature = steroid hormone (derived from cholesterol). Function = binds mineralocorticoid receptor (nuclear receptor) in collecting duct principal cells → increases ENaC and Na+/K+ ATPase transcription → Na+ reabsorption, K+ and H+ secretion → water follows Na+ → blood volume and BP increase. Stimuli for aldosterone release: angiotensin II (main), high plasma K+ (direct), ACTH (minor). Key: renin is upstream in the pathway; aldosterone is downstream. Renin leads to angiotensin II which triggers aldosterone release. Together they form the RAAS cascade.
3. What is erythropoietin and how is it regulated? ⌄
Erythropoietin (EPO): glycoprotein hormone (~34 kDa). Produced by: peritubular interstitial cells (fibroblasts) in kidney cortex (85-90%) and hepatocytes (~15%). Regulation: tissue hypoxia (low O2) is the primary stimulus. Mechanism: HIF pathway: Normally: PHD enzymes (prolyl hydroxylases) hydroxylate HIF-1alpha → binds VHL protein → ubiquitinated → proteasomal degradation. Under hypoxia: PHDs less active (require O2) → HIF-1alpha not hydroxylated → escapes degradation → enters nucleus → binds HRE (hypoxia response element) in EPO gene → EPO transcription increases. EPO action: binds EpoR on burst-forming unit-erythroid (BFU-E) and CFU-E (colony-forming unit-erythroid) progenitors → JAK2-STAT5 signalling → survival + proliferation + differentiation → pro-erythroblasts → erythroblasts → reticulocytes → RBCs. Time: 5-7 days from EPO stimulus to new circulating RBCs. Clinical applications: recombinant human EPO (epoetin alpha): CKD anaemia, cancer-related anaemia, premature infant anaemia. Darbepoetin alfa: longer-acting. Biosimilars available. Sports doping: EPO or blood transfusion to increase RBC mass and O2-carrying capacity.
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