Regarding the mechanism of action of antihypertensive drugs, all of the following statements are correct EXCEPT:

Explanation

## Mechanism Analysis of Antihypertensive Classes ### Correct Statements (Options 0, 1, 3) **Option 0 — ACE Inhibitors:** - Block angiotensin-converting enzyme, preventing conversion of angiotensin I → angiotensin II - Reduce vasoconstriction (angiotensin II is a potent vasoconstrictor) - Decrease aldosterone secretion → reduce sodium and water retention - ✓ **Correct mechanism** **Option 1 — Beta-blockers:** - Decrease heart rate (negative chronotropic effect) - Decrease cardiac contractility (negative inotropic effect) - Reduce cardiac output = Stroke Volume × Heart Rate - Blood pressure = Cardiac Output × Systemic Vascular Resistance - ✓ **Correct mechanism** **Option 3 — Thiazide Diuretics:** - Primary mechanism: ↓ intravascular volume → ↓ preload → ↓ cardiac output - Secondary mechanism: direct vasodilation of arterioles (mechanism not fully understood, but well-established) - ✓ **Correct mechanism** ### Incorrect Statement (Option 2) — Calcium Channel Blockers **Key Point:** Calcium channel blockers **DO NOT increase glomerular filtration rate (GFR)**. In fact: - They cause vasodilation of afferent arterioles (↓ intraglomerular pressure) - They may slightly reduce or maintain GFR - They are **renoprotective** in hypertension and diabetes - ~~Increase GFR~~ — this is the trap **High-Yield:** CCBs are preferred in patients with chronic kidney disease or diabetes because they: - Dilate afferent arterioles preferentially - Reduce glomerular hyperfiltration - Slow progression of renal disease - Do NOT cause hyperkalemia (unlike ACE-I/ARB) **Clinical Pearl:** ACE inhibitors and ARBs (which preferentially dilate efferent arterioles) are the true renoprotective agents in CKD and diabetes. CCBs are neutral to slightly beneficial but do not increase GFR. ## Summary Table | Drug Class | Primary Mechanism | Effect on GFR | Renal Protection | |---|---|---|---| | ACE-I / ARB | ↓ Angiotensin II | ↓ GFR initially, then stabilizes | ✓ Yes (efferent dilation) | | Beta-blocker | ↓ CO, ↓ HR | Neutral | Neutral | | CCB | Vasodilation (afferent > efferent) | Maintained or ↓ slightly | ✓ Yes (afferent protection) | | Thiazide | ↓ Volume + vasodilation | Neutral to ↓ | Neutral | [cite:KD Tripathi 8e Ch 31]