This is the activity of Atrial Natriuretic peptide (ANP)

Correct Answer: D

Rationale: ANP inhibits aldosterone/ADH, reducing water/Na+ reabsorption all apply. This defines natriuretic effect, key for volume reduction, contrasting with single actions.

Correct Answer: B

Rationale: Untreated -10 mmHg NFP leads to acute renal failure (ARF) no filtration (e.g., shock) causes acute injury, oliguria. Chronic kidney disease is progressive not acute. Diuresis needs filtration opposite here. Stable GFR requires positive NFP unfeasible. ARF's acute onset distinguishes it, key to hypoperfusion consequences, unlike chronic, diuretic, or stable outcomes.

Correct Answer: D

Rationale: ADH doesn't directly affect sodium reabsorption targets water via aquaporins (e.g., collecting duct). Increased GFR raises Na filtration reabsorption adjusts. Aldosterone boosts Na retention ENaC channels. Natriuretic hormone inhibits Na reabsorption e.g., ANP. ADH's water focus distinguishes it, key to osmolality, unlike GFR, hormonal Na regulators.

Correct Answer: C

Rationale: High glomerular pressure stems from afferent arterioles' larger diameter than efferent resistance creates ~55 mmHg (e.g., filtration drive). Low oncotic pressure opposes incorrect. High capsular pressure (~15 mmHg) resists not causes. Thick basement membrane filters doesn't raise pressure. Arteriolar disparity distinguishes it, key to GFR, unlike opposing or structural factors.

Correct Answer: C

Rationale: The myogenic mechanism is vessels' intrinsic constriction to high pressure autoregulates GFR (e.g., afferent stretch). Hormonal control (e.g., angiotensin) is extrinsic renin-driven. Sympathetic control uses nerves reduces GFR. Tubuloglomerular feedback is macula densa NaCl-based. Intrinsic response distinguishes it, key to vascular autoregulation, unlike extrinsic or feedback controls.