CHS Pathophysiology of Hypertension 2 — Questions and Answers
Question 1: Which component of the renin-angiotensin-aldosterone system (RAAS) directly causes vasoconstriction and stimulates aldosterone release?
- Renin
- Angiotensin I
- Angiotensin II (Correct answer)
- Aldosterone
Correct answer: Angiotensin II
Angiotensin II is the primary effector of the RAAS, directly causing potent vasoconstriction via AT1 receptors and stimulating aldosterone secretion from the adrenal cortex.
Question 2: In essential hypertension, increased sympathetic nervous system activity contributes to elevated blood pressure primarily through which mechanism?
- Decreased cardiac output
- Increased renal sodium retention and peripheral vasoconstriction (Correct answer)
- Reduced renin secretion
- Decreased heart rate
Correct answer: Increased renal sodium retention and peripheral vasoconstriction
Sympathetic overactivity raises blood pressure by increasing peripheral vascular resistance through vasoconstriction and promoting renal sodium and water retention via beta-adrenergic stimulation of renin release.
Question 3: Endothelial dysfunction in hypertension is characterized by reduced bioavailability of which vasodilatory molecule?
- Endothelin-1
- Thromboxane A2
- Nitric oxide (Correct answer)
- Angiotensin II
Correct answer: Nitric oxide
Reduced nitric oxide (NO) bioavailability impairs endothelium-dependent vasodilation, a hallmark of endothelial dysfunction that both contributes to and results from hypertension.
Question 4: Which receptor subtype, when overstimulated by catecholamines, increases heart rate and cardiac contractility, contributing to hypertension?
- Alpha-1 adrenergic receptor
- Beta-1 adrenergic receptor (Correct answer)
- Muscarinic M2 receptor
- AT2 receptor
Correct answer: Beta-1 adrenergic receptor
Beta-1 adrenergic receptors in the myocardium mediate positive chronotropic and inotropic effects of catecholamines, increasing cardiac output and thus blood pressure.
Question 5: The enzyme aldosterone synthase (CYP11B2) in the adrenal zona glomerulosa converts deoxycorticosterone to aldosterone. What is the primary physiological stimulus for its increased activity in hypertension?
- Elevated serum potassium and angiotensin II (Correct answer)
- Increased serum sodium
- Decreased ACTH levels
- Elevated cortisol
Correct answer: Elevated serum potassium and angiotensin II
Aldosterone synthesis is primarily stimulated by elevated serum potassium and angiotensin II, with secondary stimulation from ACTH, all of which can be upregulated in hypertensive states.
Question 6: What is the role of endothelin-1 (ET-1) in the pathophysiology of hypertension?
- It is a potent vasodilator that reduces peripheral resistance
- It is a potent vasoconstrictor that increases vascular tone and promotes inflammation (Correct answer)
- It inhibits aldosterone secretion
- It promotes natriuresis
Correct answer: It is a potent vasoconstrictor that increases vascular tone and promotes inflammation
Endothelin-1 is the most potent endogenous vasoconstrictor known, acting on ETA receptors to increase vascular smooth muscle tone, promote inflammation, and contribute to vascular remodeling in hypertension.
Question 7: In the context of hypertension, activation of mineralocorticoid receptors by aldosterone in the kidney's collecting duct causes blood pressure elevation primarily by:
- Increasing urinary sodium excretion
- Increasing water excretion
- Promoting sodium reabsorption and potassium excretion, expanding plasma volume (Correct answer)
- Inhibiting ADH action
Correct answer: Promoting sodium reabsorption and potassium excretion, expanding plasma volume
Aldosterone binds mineralocorticoid receptors in the collecting duct to upregulate ENaC and Na+/K+-ATPase, promoting sodium retention and potassium excretion, which increases plasma volume and blood pressure.
CHS Pathophysiology of Hypertension 2
Which component of the renin-angiotensin-aldosterone system (RAAS) directly causes vasoconstriction and stimulates aldosterone release?