Antihypertensive Medications – Study Notes

The ABCD of Blood Pressure Drugs

• A – ACE inhibitors & ARBs

  • ACE inhibitors (“-prils”)

  • ARBs (“-sartans”)

  • Both act on the renin-angiotensin-aldosterone system (RAAS) but at different steps.

• B – Beta Blockers (“-lols”)

  • Lower BP by blocking sympathetic stimulation of the heart.

  • Not first-line for most patients due to less protection against stroke/mortality in those >60.

• C – Calcium Channel Blockers (CCBs)

  • Dihydropyridines (“-dipines”): primarily act on vascular smooth muscle (vasodilation).

  • Non-dihydropyridines: act more on the heart (decrease HR, conduction, contractility).

• D – Diuretics (Thiazide & Thiazide-like)

  • Often have “thiazide” in the name.

  • Work in the distal convoluted tubule, blocking Na⁺/Cl⁻ reabsorption.

Blood Pressure Equation

$$BP = Cardiac Output (CO) \times Systemic Vascular Resistance (SVR)$$

• CO = HR × Stroke Volume

• Factors that raise BP:

  • ↑ Sympathetic stimulation (↑HR, ↑contractility)

  • ↑ Blood volume (↑stroke volume)

  • ↑ SVR (vasoconstriction or ↑ blood viscosity)

Mechanisms of Action

A – ACE inhibitors & ARBs

• RAAS Pathway:

  • ↓ Renal perfusion → kidneys release renin → converts angiotensinogen → angiotensin I.

  • ACE (lungs) converts angiotensin I → angiotensin II.

  • Angiotensin II effects:

    • Vasoconstriction (↑SVR)

    • Aldosterone release (Na⁺ & water retention)

    • ADH release (↑ water reabsorption)

    • Net: ↑ Blood pressure.

• ACE inhibitors block conversion to angiotensin II.

• ARBs block angiotensin II receptors.

• Net effect: vasodilation + ↓ fluid retention → ↓ BP.

B – Beta Blockers

• Block β-adrenergic receptors (sympathetic system).

• β1 (heart): ↓ HR, ↓ contractility → ↓ CO.

• β2 (lungs/vascular smooth muscle): relaxation/bronchodilation (but blockade may cause bronchospasm).

• Not usually first-line for uncomplicated HTN, but used when comorbidities exist (e.g., post-MI, heart failure, arrhythmias).

C – Calcium Channel Blockers

• Calcium influx normally: excitable cells contract (muscle) or conduct (neurons).

• CCBs block calcium entry.

  • Dihydropyridines (e.g., amlodipine, nifedipine):

    • Vasodilators (↓ SVR → ↓ BP).

  • Non-dihydropyridines (e.g., verapamil, diltiazem):

    • Slow SA/AV node conduction → ↓ HR, ↓ contractility.

D – Thiazide & Thiazide-like Diuretics

• Act on distal convoluted tubule.

• Block Na⁺/Cl⁻ symporter → more Na⁺ & Cl⁻ excreted → water follows → ↓ blood volume → ↓ BP.

• Side effects/considerations:

  • ↑ Calcium reabsorption → good for osteoporosis.

  • K⁺ loss → risk of hypokalemia.

  • Volume depletion.

Key Points

• First-line classes for HTN:

  • ACE inhibitors / ARBs

  • CCBs

  • Thiazide diuretics

• Beta blockers: not first-line unless specific indication (HF, CAD, arrhythmia).

• All act on CO or SVR via different mechanisms.