Angiotensin II receptors and actions US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Angiotensin II receptors and actions. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Angiotensin II receptors and actions US Medical PG Question 1: Which receptor type mediates the slow phase of synaptic transmission in autonomic ganglia?
- A. Muscarinic (M3)
- B. Muscarinic (M2)
- C. Muscarinic (M1) (Correct Answer)
- D. Nicotinic (N2)
Angiotensin II receptors and actions Explanation: ***Muscarinic (M1)***
- **M1 receptors** are **Gq-protein coupled receptors** that activate phospholipase C, leading to increased intracellular calcium and diacylglycerol, which mediates the slow excitatory postsynaptic potential in autonomic ganglia.
- This activation results in a **slow depolarization** that prolongs the excitability of ganglionic neurons after the initial fast synaptic transmission.
*Muscarinic (M3)*
- **M3 receptors** are primarily found on **smooth muscle**, glands, and endothelium, mediating contraction, secretion, and vasodilation, respectively.
- While also **Gq-protein coupled**, their role in autonomic ganglia is not the main mediator of the slow phase of synaptic transmission.
*Muscarinic (M2)*
- **M2 receptors** are **Gi-protein coupled receptors** mainly found in the heart, mediating decreased heart rate and contractility.
- In autonomic ganglia, M2 receptors could have a modulatory role, but they are not responsible for the slow excitatory phase of synaptic transmission.
*Nicotinic (N2)*
- **Nicotinic N2 receptors** (also known as **NN or neuronal nicotinic receptors**) mediate the **fast excitatory postsynaptic potential** (EPSP) in autonomic ganglia by opening ion channels.
- This leads to rapid depolarization and action potential generation, which is distinct from the **slower, prolonged phase** of transmission.
Angiotensin II receptors and actions US Medical PG Question 2: An investigator is studying patients with acute decompensated congestive heart failure. He takes measurements of a hormone released from atrial myocytes, as well as serial measurements of left atrial and left ventricular pressures. The investigator observes a positive correlation between left atrial pressures and the serum level of this hormone. Which of the following is most likely the mechanism of action of this hormone?
- A. Increases potassium excretion at the collecting ducts
- B. Constricts afferent renal arteriole
- C. Decreases sodium reabsorption at the collecting tubules (Correct Answer)
- D. Decreases reabsorption of bicarbonate in the proximal convoluted tubules
- E. Increases free water reabsorption from the distal tubules
Angiotensin II receptors and actions Explanation: ***Decreases sodium reabsorption at the collecting tubules***
- The hormone described, exhibiting a positive correlation with left atrial pressure and released from atrial myocytes, is **Atrial Natriuretic Peptide (ANP)**.
- ANP promotes **natriuresis** (sodium excretion) and **diuresis** by directly inhibiting sodium reabsorption in the collecting tubules, thereby reducing blood volume and cardiac preload.
*Increases potassium excretion at the collecting ducts*
- While ANP does promote fluid and electrolyte excretion, its primary effect is on sodium and water, not a direct increase in **potassium excretion**. **Aldosterone**, not ANP, primarily increases potassium secretion in the collecting ducts.
- This option describes a mechanism more consistent with **mineralocorticoid activity**, which is counteracted by ANP.
*Constricts afferent renal arteriole*
- ANP generally causes **vasodilation** of the afferent arteriole and constriction of the efferent arteriole, increasing glomerular filtration rate (GFR).
- **Angiotensin II** is a primary constrictor of the afferent and efferent renal arterioles, which is the opposite effect of ANP.
*Decreases reabsorption of bicarbonate in the proximal convoluted tubules*
- This mechanism is primarily involved in **acid-base balance** and is influenced by factors like parathyroid hormone or respiratory/metabolic acidosis/alkalosis.
- ANP's main action is on **sodium and water balance**, not directly on bicarbonate reabsorption.
*Increases free water reabsorption from the distal tubules*
- **Vasopressin (Antidiuretic Hormone, ADH)** is responsible for increasing free water reabsorption in the distal tubules and collecting ducts.
- ANP's action is to *increase* water excretion, working in opposition to ADH to reduce circulating fluid volume.
Angiotensin II receptors and actions US Medical PG Question 3: A 64-year-old African American female comes to the physician's office for a routine check-up. The patient's past medical history is significant for hypertension, diabetes, and osteoarthritis in her right knee. Her medications include metformin, glimepiride, lisinopril, metoprolol, hydrochlorothiazide, and ibuprofen as needed. Her only complaint is an unremitting cough that started about 3 weeks ago and she has noticed some swelling around her mouth. The drug most likely responsible for her recent symptoms causes its primary renal hemodynamic effect on which part of the kidney?
- A. Collecting duct
- B. Distal convoluted tubule
- C. Juxtaglomerular cells
- D. Efferent arteriole (Correct Answer)
- E. Afferent arteriole
Angiotensin II receptors and actions Explanation: ***Efferent arteriole***
- The patient's symptoms of an **unremitting cough** and **angioedema** (swelling around her mouth) are classic side effects of **ACE inhibitors**, such as **lisinopril**.
- ACE inhibitors primarily exert their renal hemodynamic effects by **dilating the efferent arteriole**, leading to a decrease in intraglomerular pressure and glomerular filtration rate.
*Collecting duct*
- The collecting duct is the primary site of action for **vasopressin (ADH)** and **aldosterone**, regulating water and sodium reabsorption, respectively.
- While other medications like **thiazides** (used by the patient) affect distal tubules and collecting ducts indirectly, their direct impact on the collecting duct is not the cause of angioedema or cough.
*Distal convoluted tubule*
- The distal convoluted tubule is the main site of action for **thiazide diuretics** (e.g., hydrochlorothiazide), which inhibit the Na-Cl cotransporter.
- This tubule segment is not directly involved in the mechanism leading to angioedema or cough caused by ACE inhibitors.
*Juxtaglomerular cells*
- Juxtaglomerular cells are responsible for producing **renin**, which is the initial step in the **renin-angiotensin-aldosterone system (RAAS)**.
- While ACE inhibitors block the conversion of angiotensin I to angiotensin II, they do not directly act on the juxtaglomerular cells themselves to cause their side effects.
*Afferent arteriole*
- The afferent arteriole is primarily regulated by **sympathetic tone** and local factors, and is the main site of action for medications like **NSAIDs** (e.g., ibuprofen, which the patient takes as needed).
- While NSAIDs cause **afferent arteriole constriction** and can impair renal function, they do not cause angioedema or a chronic cough.
Angiotensin II receptors and actions US Medical PG Question 4: A new drug X is being tested for its effect on renal function. During the experiments, the researchers found that in patients taking substance X, the urinary concentration of sodium decreases while urine potassium concentration increase. Which of the following affects the kidneys in the same way as does substance X?
- A. Aldosterone (Correct Answer)
- B. Furosemide
- C. Spironolactone
- D. Atrial natriuretic peptide
- E. Hydrochlorothiazide
Angiotensin II receptors and actions Explanation: ***Aldosterone***
- **Aldosterone** acts on the **principal cells** of the **collecting duct** to increase sodium reabsorption and potassium secretion.
- This action leads to a decrease in urinary sodium concentration and an increase in urinary potassium concentration, matching the effects of drug X.
*Furosemide*
- **Furosemide** is a **loop diuretic** that inhibits the **Na-K-2Cl cotransporter** in the **thick ascending limb** of the loop of Henle.
- This inhibition leads to increased excretion of sodium, potassium, and water, resulting in higher urinary sodium concentration.
*Spironolactone*
- **Spironolactone** is an **aldosterone antagonist** that blocks aldosterone's effects on the collecting duct.
- This leads to increased sodium excretion and decreased potassium excretion (potassium-sparing effect), which is the opposite of drug X.
*Atrial natriuretic peptide*
- **Atrial natriuretic peptide (ANP)** is released in response to atrial stretch and causes **natriuresis** (increased sodium excretion) and **diuresis**.
- It works by dilating afferent arterioles and constricting efferent arterioles, increasing GFR, and inhibiting sodium reabsorption, thus increasing urinary sodium concentration.
*Hydrochlorothiazide*
- **Hydrochlorothiazide** is a **thiazide diuretic** that inhibits the **Na-Cl cotransporter** in the **distal convoluted tubule**.
- This leads to increased sodium and chloride excretion but typically causes potassium wasting (hypokalemia), which differs from the increased urinary potassium concentration seen with drug X.
Angiotensin II receptors and actions US Medical PG Question 5: A 69-year-old man with hypertension and congestive heart failure is brought to the emergency department because of a 9-day history of worsening shortness of breath and swelling of his legs. His respirations are 25/min, and blood pressure is 160/98 mm Hg. Pulse oximetry on 5 L O2 via nasal cannula shows an oxygen saturation of 92%. Examination shows 2+ pretibial edema bilaterally. Crackles are heard at both lung bases. ACE inhibitors are being considered for this patient's treatment. The enzyme that these medications inhibit, which is responsible for bradykinin breakdown, is primarily produced in which of the following?
- A. Pulmonary endothelium (Correct Answer)
- B. Atria
- C. Juxtaglomerular cells
- D. Zona glomerulosa
- E. Liver
Angiotensin II receptors and actions Explanation: ***Pulmonary endothelium***
- The **pulmonary endothelium** is rich in **angiotensin-converting enzyme (ACE)**, which is responsible for the breakdown of **bradykinin**.
- Medications like **ACE inhibitors** block this enzyme, leading to increased bradykinin levels, which can cause side effects like **cough** and **angioedema**.
*Atria*
- The **atria** produce **atrial natriuretic peptide (ANP)** in response to stretch, which plays a role in fluid and electrolyte balance but not directly in bradykinin breakdown.
- ANP promotes **vasodilation** and **natriuresis**, contributing to blood pressure regulation.
*Juxtaglomerular cells*
- **Juxtaglomerular cells** in the kidney produce **renin**, an enzyme that initiates the **renin-angiotensin-aldosterone system** by converting angiotensinogen to angiotensin I.
- Renin production is stimulated by reduced renal perfusion pressure, sympathetic activity, and decreased sodium delivery to the macula densa.
*Zona glomerulosa*
- The **zona glomerulosa** of the adrenal cortex produces **aldosterone**, a mineralocorticoid that regulates sodium and potassium balance.
- Aldosterone's primary role is in salt and water retention, and it does not directly participate in bradykinin metabolism.
*Liver*
- The **liver** is involved in the synthesis of many plasma proteins, clotting factors, and detoxification processes, but it is not the primary site for bradykinin breakdown.
- While the liver metabolizes many substances, **ACE activity** for bradykinin degradation is concentrated in the pulmonary endothelium.
Angiotensin II receptors and actions US Medical PG Question 6: Activation of the renin-angiotensin-aldosterone system yields a significant physiological effect on renal blood flow and filtration. Which of the following is most likely to occur in response to increased levels of Angiotensin-II?
- A. Decreased renal plasma flow, decreased filtration fraction
- B. Decreased renal plasma flow, increased glomerular capillary oncotic pressure
- C. Increased renal plasma flow, decreased filtration fraction
- D. Increased renal plasma flow, increased filtration fraction
- E. Decreased renal plasma flow, increased filtration fraction (Correct Answer)
Angiotensin II receptors and actions Explanation: ***Decreased renal plasma flow, increased filtration fraction***
- **Angiotensin II** causes **efferent arteriolar constriction**, which reduces blood flow leaving the glomerulus, thereby **decreasing renal plasma flow**.
- This efferent constriction also increases **glomerular hydrostatic pressure** and reduces plasma flow distal to the glomerulus, leading to a **higher filtration fraction** (GFR/RPF).
*Decreased renal plasma flow, decreased filtration fraction*
- While **renal plasma flow decreases**, a **decreased filtration fraction** would imply that either GFR decreases disproportionately more than RPF or GFR does not increase despite the RPF reduction, which is not the typical response to **angiotensin II** due to its predominant effect on the **efferent arteriole**.
*Decreased renal plasma flow, increased glomerular capillary oncotic pressure*
- **Increased glomerular capillary oncotic pressure** is a consequence of increased filtration fraction, as more fluid is filtered out, leaving behind a more concentrated plasma. This option includes a correct element (decreased RPF) but pairs it with a less direct and defining outcome of acute Angiotensin II action as the primary physiological effect.
*Increased renal plasma flow, decreased filtration fraction*
- **Angiotensin II** causes **vasoconstriction**, predominantly of the efferent arteriole, which by definition would **decrease renal plasma flow**, not increase it.
- A **decreased filtration fraction** would be inconsistent with efferent arteriolar constriction which typically raises GFR relative to RPF.
*Increased renal plasma flow, increased filtration fraction*
- **Angiotensin II** causes **vasoconstriction**, leading to a **decrease in renal plasma flow**, not an increase.
- While **filtration fraction is increased**, the initial premise of increased renal plasma flow is incorrect.
Angiotensin II receptors and actions US Medical PG Question 7: A physician is choosing whether to prescribe losartan or lisinopril to treat hypertension in a 56-year-old male. Relative to losartan, one would expect treatment with lisinopril to produce which of the following changes in the circulating levels of these peptides?
- A. Aldosterone increase; bradykinin decrease
- B. Angiotensin II increase; bradykinin decrease
- C. Renin decrease; angiotensin I increase
- D. Bradykinin increase; angiotensin II decrease (Correct Answer)
- E. Renin decrease; angiotensin II increase
Angiotensin II receptors and actions Explanation: ***Bradykinin increase; angiotensin II decrease***
- **Lisinopril** is an **ACE inhibitor**, which directly blocks the conversion of **angiotensin I** to **angiotensin II**, leading to a decrease in circulating **angiotensin II** levels.
- ACE is also responsible for the breakdown of **bradykinin**, so inhibiting ACE with lisinopril will lead to an **increase in bradykinin** levels, contributing to vasodilation but also the characteristic cough.
*Aldosterone increase; bradykinin decrease*
- **Lisinopril** (an ACE inhibitor) decreases **angiotensin II**, which in turn leads to a **decrease in aldosterone** synthesis and release, not an increase.
- **Bradykinin** levels would increase due to ACE inhibition, as ACE is involved in its degradation.
*Angiotensin II increase; bradykinin decrease*
- **Lisinopril** directly inhibits the enzyme responsible for producing **angiotensin II**, thus leading to its **decrease**, not an increase.
- **Bradykinin** levels would increase because its degradation pathway (via ACE) is blocked, not decrease.
*Renin decrease; angiotensin I increase*
- **Lisinopril** reduces the negative feedback on **renin** release, leading to an **increase in renin** levels, not a decrease.
- While ACE is inhibited by lisinopril, this leads to an accumulation of its substrate, **angiotensin I**, resulting in an increase of angiotensin I.
*Renin decrease; angiotensin II increase*
- As an ACE inhibitor, lisinopril would lead to an **increase in renin** due to reduced negative feedback from angiotensin II, not a decrease.
- **Angiotensin II** levels would **decrease** because its production from angiotensin I is directly inhibited by lisinopril.
Angiotensin II receptors and actions US Medical PG Question 8: A 71-year-old African American man diagnosed with high blood pressure presents to the outpatient clinic. In the clinic, his blood pressure is 161/88 mm Hg with a pulse of 88/min. He has had similar blood pressure measurements in the past, and you initiate captopril. He presents back shortly after initiation with extremely swollen lips, tongue, and face. After captopril is discontinued, what is the most appropriate step for the management of his high blood pressure?
- A. Initiate a beta-blocker
- B. Switch to ramipril
- C. Initiate a thiazide diuretic (Correct Answer)
- D. Reinitiate captopril
- E. Initiate an ARB
Angiotensin II receptors and actions Explanation: ***Initiate a thiazide diuretic***
- The patient experienced **angioedema** after taking **captopril**, which is an **ACE inhibitor**. This is a life-threatening adverse effect, and it indicates that all **ACE inhibitors** should be avoided in the future.
- Due to the risk of angioedema, a different class of antihypertensive should be used. Given his African American ethnicity, a **thiazide diuretic** or **calcium channel blocker** would be an appropriate initial choice for monotherapy if hypertension is stage 1, or combination therapy if stage 2 hypertension, otherwise, a second agent, such as a **calcium channel blocker**, can be added.
*Initiate a beta-blocker*
- While beta-blockers are a class of antihypertensive drugs, they are generally not preferred as **first-line monotherapy** for **hypertension**, especially in older African American patients, unless there are specific comorbidities like heart failure or coronary artery disease.
- The most appropriate first-line choice after **ACE inhibitor-induced angioedema** would be a thiazide diuretic or calcium channel blocker, as per ACC/AHA guidelines for primary hypertension.
*Switch to ramipril*
- **Ramipril** is also an **ACE inhibitor**, and the patient experienced **angioedema** with **captopril** (another ACE inhibitor).
- Cross-reactivity and recurrence of angioedema are high with other ACE inhibitors, making this choice extremely dangerous and contraindicated.
*Reinitiate captopril*
- The patient developed **angioedema**, a severe and potentially fatal hypersensitivity reaction, to **captopril**.
- Reinitiating the same drug could lead to recurrent, and potentially more severe, angioedema and is therefore absolutely contraindicated.
*Initiate an ARB*
- **Angiotensin receptor blockers (ARBs)**, while a different class from ACE inhibitors, act on the renin-angiotensin system and carry a **small but significant risk of cross-reactivity** leading to angioedema, especially in patients who have experienced it with an ACE inhibitor.
- Given the life-threatening nature of angioedema, it is generally recommended to avoid ARBs if a patient has a history of ACE inhibitor-induced angioedema.
Angiotensin II receptors and actions US Medical PG Question 9: A 48-year-old woman comes to the physician for a follow-up examination. At her visit 1 month ago, her glomerular filtration rate (GFR) was 100 mL/min/1.73 m2 and her renal plasma flow (RPF) was 588 mL/min. Today, her RPF is 540 mL/min and her filtration fraction (FF) is 0.2. After her previous appointment, this patient was most likely started on a drug that has which of the following effects?
- A. Inhibition of the renal Na-K-Cl cotransporter
- B. Constriction of the afferent arteriole
- C. Relaxation of urinary smooth muscle
- D. Constriction of the efferent arteriole (Correct Answer)
- E. Inhibition of vasopressin
Angiotensin II receptors and actions Explanation: ***Constriction of the efferent arteriole***
- The previous GFR was 100 mL/min and RPF was 588 mL/min. For the follow-up, RPF is 540 mL/min and FF is 0.2. The new GFR can be calculated as FF × RPF = 0.2 × 540 = **108 mL/min**.
- The patient shows **increased GFR** (100→108 mL/min) with **decreased RPF** (588→540 mL/min), resulting in an **increased filtration fraction**.
- Medications that **constrict the efferent arteriole**, such as **NSAIDs**, produce this pattern by blocking prostaglandin synthesis. Prostaglandins normally cause vasodilation (predominantly of the afferent arteriole). When blocked, there is relatively more **efferent arteriolar constriction**, which increases glomerular hydrostatic pressure, thereby **increasing GFR while reducing overall RPF**.
*Inhibition of the renal Na-K-Cl cotransporter*
- This effect describes **loop diuretics** (e.g., furosemide), which increase sodium excretion and water diuresis.
- Loop diuretics typically cause a **decrease in GFR** due to reduced fluid volume and lower filtration pressure, which contradicts the slight increase in GFR observed.
*Constriction of the afferent arteriole*
- **Afferent arteriole constriction** (e.g., by NSAIDs in high doses or norepinephrine) would decrease blood flow into the glomerulus, leading to a **decrease in both RPF and GFR**.
- While RPF decreased in this case, GFR actually increased, making this option incorrect.
*Relaxation of urinary smooth muscle*
- Relaxation of urinary smooth muscle is characteristic of drugs like **alpha-blockers** (e.g., tamsulosin) or antimuscarinics used for conditions like benign prostatic hyperplasia or overactive bladder.
- This effect primarily impacts urine flow out of the bladder and does **not directly affect GFR or RPF** in the way described.
*Inhibition of vasopressin*
- Vasopressin (ADH) inhibition leads to **increased water excretion** and is seen with drugs like **vasopressin receptor antagonists** (vaptans) or ethanol.
- While it affects fluid balance, it typically causes a **decrease in GFR** due to hypovolemia and has no direct mechanism to increase GFR with decreased RPF as observed.
Angiotensin II receptors and actions US Medical PG Question 10: A 75-year-old woman is brought to a physician’s office by her son with complaints of diarrhea and vomiting for 1 day. Her stool is loose, watery, and yellow-colored, while her vomitus contains partially digested food particles. She denies having blood or mucus in her stools and vomitus. Since the onset of her symptoms, she has not had anything to eat and her son adds that she is unable to tolerate fluids. The past medical history is unremarkable and she does not take any medications regularly. The pulse is 115/min, the respiratory rate is 16/min, the blood pressure is 100/60 mm Hg, and the temperature is 37.0°C (98.6°F). The physical examination shows dry mucous membranes and slightly sunken eyes. The abdomen is soft and non-tender. Which of the following physiologic changes in glomerular filtration rate (GFR), renal plasma flow (RPF), and filtration fraction (FF) are expected?
- A. Decreased GFR, decreased RPF, decreased FF
- B. Decreased GFR, decreased RPF, no change in FF
- C. Increased GFR, increased RPF, increased FF
- D. Increased GFR, decreased RPF, increased FF
- E. Decreased GFR, decreased RPF, increased FF (Correct Answer)
Angiotensin II receptors and actions Explanation: ***Decreased GFR, decreased RPF, increased FF***
- Due to **dehydration** from diarrhea and vomiting, there is a decrease in blood volume leading to decreased renal blood flow and **renal plasma flow (RPF)**.
- The body responds to hypovolemia by activating the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system, which cause **preferential efferent arteriolar constriction** (more than afferent constriction). This helps maintain glomerular hydrostatic pressure despite reduced renal perfusion.
- As a result, **GFR decreases** but proportionally **less than RPF decreases**, causing the **filtration fraction (FF = GFR/RPF) to increase**.
- In this patient with significant dehydration (tachycardia, hypotension, dry mucous membranes), both GFR and RPF are reduced, but FF is elevated due to compensatory mechanisms.
*Decreased GFR, decreased RPF, decreased FF*
- While GFR and RPF will decrease due to dehydration, the **filtration fraction is expected to increase**, not decrease.
- A decreased FF would imply GFR fell proportionally more than RPF, which contradicts the physiologic response where efferent arteriolar constriction helps preserve GFR relative to RPF.
*Decreased GFR, decreased RPF, no change in FF*
- With significant fluid loss and compensatory mechanisms (efferent arteriolar constriction via angiotensin II), a change in **filtration fraction** is expected.
- The body actively alters arteriolar tone to prioritize GFR maintenance, which directly increases FF.
*Increased GFR, increased RPF, increased FF*
- This pattern suggests **hypervolemia** or increased renal perfusion, which directly contradicts the patient's severe dehydration.
- Both GFR and RPF are expected to decrease in volume depletion, not increase.
*Increased GFR, decreased RPF, increased FF*
- An increase in GFR is physiologically impossible given the patient's severe volume depletion and reduced renal perfusion.
- While FF does increase in dehydration, this occurs in the context of **both GFR and RPF being decreased**, not with an increased GFR.
More Angiotensin II receptors and actions US Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
