QUIZ : Renal physiology and blood pressure regulation

A 10-question quiz on renal physiology and blood pressure regulation, focusing on RAAS, nephron function, sympathetic tone, and antihypertensive drug mechanisms.

 

1. A healthy 25-year-old runs a half marathon on a hot day and becomes mildly dehydrated. Which mechanism is most likely to be activated to conserve circulating volume and maintain blood pressure?
   
   A. Increased atrial natriuretic peptide (ANP) release
   B. Decreased sympathetic nervous activity
   C. Renin release from juxtaglomerular cells
   D. Inhibition of antidiuretic hormone (ADH) secretion
   E. Afferent arteriolar vasodilation due to high perfusion
   Explanation: Dehydration reduces effective circulating volume → renal perfusion drops → JG cells release renin → RAAS is activated to raise BP and conserve fluid. ANP and ADH would act in the opposite direction, and sympathetic activity would be increased, not decreased.


2. A patient is given a drug that selectively dilates the efferent arteriole of the glomerulus. What is the most likely short-term effect on glomerular filtration rate (GFR)?
   
   A. GFR increases due to improved renal blood flow
   B. GFR decreases due to reduced hydrostatic pressure in the glomerulus
   C. GFR is unchanged due to autoregulation
   D. GFR increases due to myogenic afferent constriction
   E. GFR decreases because sodium delivery to the macula densa increases
   Explanation: Dilation of the efferent arteriole lowers the pressure in the glomerular capillaries → GFR falls. This is relevant to ACE inhibitors, which reduce efferent arteriole tone via reduced angiotensin II.


3. A 60-year-old man has persistently high blood pressure. His investigation shows overactivity of the RAAS. Which of the following would help break the cycle of volume retention and vasoconstriction?
   
   A. Giving synthetic ADH
   B. Prescribing a mineralocorticoid receptor agonist
   C. Blocking angiotensin II receptors
   D. Administering intravenous sodium chloride
   E. Stimulating the sympathetic nervous system
   Explanation: Overactive RAAS leads to vasoconstriction and aldosterone-driven volume retention. ARBs block angiotensin II at its receptor, addressing both issues. The other options would worsen hypertension or bypass the core mechanism.


4. A healthy person stands up quickly after lying down. There's a brief drop in blood pressure, but it recovers within seconds. Which system is most immediately responsible for this recovery?
   
   A. Increased secretion of aldosterone
   B. Activation of the renin–angiotensin–aldosterone system
   C. Suppression of atrial natriuretic peptide release
   D. Stimulation of the sympathetic nervous system
   E. Release of ADH to conserve free water
   Explanation: On standing, baroreceptors sense a transient drop in pressure and trigger a sympathetic reflex, increasing heart rate and peripheral vasoconstriction. RAAS and ADH contribute later, but sympathetic tone corrects the BP fastest.


5. A researcher blocks sodium detection at the macula densa in an animal model. Which of the following changes would most likely occur?
   
   A. Increased afferent arteriole constriction
   B. Decreased renin release from the JG apparatus
   C. Decreased GFR due to enhanced tubuloglomerular feedback
   D. Increased renin secretion and dilation of the afferent arteriole
   E. No change, as the macula densa is unrelated to BP control
   Explanation: The macula densa detects sodium chloride delivery. If this sensing is blocked or sodium is low, it interprets it as reduced perfusion → triggers afferent vasodilation and stimulates renin release to restore BP.


6. A first-year student is revising ACE inhibitors and wonders: “What makes them such a cornerstone in managing hypertension?” Which of the following best explains their antihypertensive effect?
   
   A. Blocking sodium channels in the proximal tubule
   B. Increasing sympathetic tone to afferent arterioles
   C. Inhibiting aldosterone synthesis in the adrenal cortex
   D. Preventing conversion of angiotensin I to angiotensin II
   E. Stimulating water reabsorption via ADH pathways
   Explanation: ACE inhibitors stop the key enzymatic step that forms angiotensin II — a potent vasoconstrictor that also drives aldosterone and ADH release. Blocking it reduces vascular tone and fluid retention.


7. A student asks why combining an ACE inhibitor and a loop diuretic is effective in heart failure. What do these drugs target together?
   
   A. Proximal tubular bicarbonate and potassium
   B. Sodium reabsorption and vasoconstriction
   C. Glomerular hydrostatic pressure and oncotic pressure
   D. Sympathetic drive and renin release
   E. Aldosterone and ADH release
   Explanation: Loop diuretics reduce volume by inhibiting sodium reabsorption. ACE inhibitors reduce vasoconstriction and aldosterone-mediated sodium retention. Together, they tackle pressure and volume.


8. Which of the following correctly pairs a drug with its site of action in the nephron?
   
   A. Spironolactone → Proximal tubule
   B. Thiazide diuretic → Thick ascending limb
   C. Loop diuretic → Collecting duct
   D. Amiloride → Cortical collecting duct
   E. Acetazolamide → Thick ascending limb
   Explanation: Amiloride is a potassium-sparing diuretic that blocks ENaC in the cortical collecting duct, reducing sodium reabsorption without causing potassium loss. ACE inhibitors act outside the nephron via hormonal modulation.


9. An experimental drug increases secretion of ANP. Which of the following changes would you expect as a result?
   
   A. Increased aldosterone secretion
   B. Afferent arteriole constriction
   C. Decreased sodium excretion
   D. Suppression of renin release
   E. Stimulation of angiotensin II production
   Explanation: ANP opposes RAAS. It promotes vasodilation, natriuresis, and suppresses renin and aldosterone secretion — making it an endogenous “brake” on fluid retention and vasoconstriction.


10. A new drug inhibits sodium reabsorption in the distal convoluted tubule. Which of the following would most likely be observed as a result?
    
    A. Reduced potassium excretion
    B. Increased water and sodium excretion
    C. Decreased aldosterone levels
    D. Increased ADH secretion
    E. Altered tubuloglomerular feedback
    Explanation: Blocking sodium reabsorption in the distal tubule (as thiazide diuretics do) leads to natriuresis and diuresis, lowering blood volume and BP. Potassium loss may also occur due to downstream effects, but sodium and water excretion are primary.

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