HTN Pharmacology

ACE-inhibitor & ARB

The liver secretes angiotensinogen which is then converted to angiotensin 1 via the action of renin (1), which is released by the kidneys.
Angiotensin 1 is subsequently converted into its active component (2) angiotensin 2 via the action of angiotensin converting enzyme, which is produced by the pulmonary vasculature.
Angiotensin 2 increases blood pressure via two mechanisms: angiotensin 2 by itself is a potent vasoconstrictor (3) which increases systemic blood pressure.
Furthermore, angiotensin 2 acts on the adrenal cortex to release aldosterone from the zona glomerulosa (4).
Aldosterone acts on the collecting ducts and distal convoluted tubules (DCT) to facilitate sodium ion reabsorption by acting on the sodium-potassium pump (5); water is also reabsorbed in conjunction with sodium ions during this process (not shown).
The reabsorption of sodium ions and water increases intravascular volume thereby increasing blood pressure

Mechanism of Action: Block the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion.
Common Side Effects: Dry cough, hyperkalemia, dizziness, angioedema, renal dysfunction.
Side effects: dry cough d/t decreased bradykinin breakdown, angioedema, risk of acute renal failure (in bilateral renal artery stenosis), hyperkalemia, teratogenic
Contraindications: Pregnancy, breastfeeding, renovascular disease (bilateral renal artery stenosis), history of angioedema, hyperkalemia.
Examples & Dosage:

Mechanism of Action: Block angiotensin II receptors, preventing vasoconstriction and aldosterone effects.
Common Side Effects: Dizziness, hyperkalemia, fatigue, angioedema (rare).
Contraindications: Pregnancy, bilateral renal artery stenosis, hyperkalemia.
Examples & Dosage:

Mechanism of Action: Inhibit calcium influx in vascular smooth muscle (dihydropyridines) or cardiac muscle (non-dihydropyridines), reducing blood pressure.
Common Side Effects:
- Dihydropyridines: Peripheral edema, flushing, headache.
- Non-dihydropyridines: Bradycardia, constipation, heart block.
Contraindications: Severe aortic stenosis, heart block (non-dihydropyridines), heart failure (non-dihydropyridines).
Examples & Dosage:

Mechanism of Action: Increase sodium and water excretion, reducing blood volume.
Types:
- Thiazide Diuretics: Hydrochlorothiazide, Chlorthalidone
- Loop Diuretics: Furosemide
- Potassium-Sparing Diuretics: Spironolactone, Amiloride
Common Side Effects:
- Thiazides: Hypokalemia, hypercalcemia, hyperuricemia.
- Loop: Hypokalemia, ototoxicity.
- Potassium-Sparing: Hyperkalemia, gynecomastia (spironolactone).
Contraindications:
- Thiazides: Gout, severe renal failure.
- Loop: Sulfa allergy (except ethacrynic acid).
- Potassium-Sparing: Hyperkalemia, anuria.
Examples & Dosage:

Mechanism of Action: Block beta-adrenergic receptors, reducing heart rate and cardiac output.
Common Side Effects: Fatigue, bradycardia, depression, erectile dysfunction.
Contraindications: Asthma, severe bradycardia, heart block, uncontrolled heart failure.
Examples & Dosage:

Mechanism of Action: Block alpha-1 adrenergic receptors, causing vasodilation.
Common Side Effects: Orthostatic hypotension, dizziness, headache, reflex tachycardia, priapism.
Contraindications: Postural hypotension, hypersensitivity.
Examples & Dosage: