The release of cortisol is stimulated by

Correct Answer: D

Rationale: Adrenocorticotropic hormone (ACTH) from the anterior pituitary stimulates adrenal cortisol release, managing stress/metabolism. Aldosterone (adrenal) and angiotensin (RAAS) regulate fluid, ADH controls water not cortisol. ACTH's specific role distinguishes it, key to the HPA axis, contrasting with fluid-regulating hormones.

Correct Answer: C

Rationale: Insulin, from pancreatic β-cells, is synthesized as proinsulin, cleaved to active form, lowering glucose via membrane receptors (tyrosine kinase). α-cells secrete glucagon, not insulin. It's a dual-chain polypeptide, not triple helical structural misfit. It binds surface receptors, not cytoplasmic steroids do that. Prohormone synthesis distinguishes insulin's production, critical for its activation and glucose regulation, unlike wrong cell origin, structure, or receptor location.

Correct Answer: D

Rationale: Erythropoietin (EPO) production from kidneys is inhibited by theophylline (adenosine antagonist), reducing RBC stimulation in hypoxia. It increases RBC via progenitor division, but takes days, not 24 hours. Inactivation is hepatic/renal, not spleen-specific. Theophylline's suppression distinguishes it, critical for EPO regulation, unlike action, inactivation, or timing claims.

Correct Answer: D

Rationale: PTH inhibits PO₄ reabsorption (increases excretion) in kidneys, lowering serum PO₄ while raising Ca²⁺ dual action defines it. PTH increases Ca reabsorption, not decreases. PO₄ secretion rises, not falls. Calcitonin reduces bone resorption. PTH's PO₄ effect distinguishes it, critical for calcium-phosphate balance, unlike Ca reabsorption, secretion, or calcitonin errors.

Correct Answer: D

Rationale: Prostaglandins (e.g., PGE2) increase renin secretion, enhancing RAAS in low perfusion/stress. Renin converts angiotensinogen to angiotensin I, but angiotensin II triggers aldosterone indirect. Conversion occurs in blood (renin), not lungs (ACE to angiotensin II). High Na at macula densa suppresses renin. Prostaglandin stimulation distinguishes it, critical for RAAS activation, unlike indirect, site, or Na errors.