Mechanism of Action of Antihypertensive Drugs on Cardiac Output

Mechanism of Action of Antihypertensive Drugs on Cardiac Output

This article will discuss the mechanisms of action of antihypertensive drugs on cardiac output, focusing on the main drug groups: diuretics, renin-angiotensin-aldosterone system (RAAS) modulators, calcium channel blockers, and cardiac glycosides.

# 1. Diuretics

• Thiazide diuretics:

• Mechanism: Inhibit the reabsorption of Na+ and Cl- in the distal convoluted tubule, increasing the excretion of water and salt.

• Side effects: Increased K+ excretion, increased Ca++ in the blood, decreased Mg++ with prolonged use.

• Loop diuretics (furosemide):

• Mechanism: Inhibit the Na+, K+, Cl- co-transporter in the ascending limb of the loop of Henle, increasing the excretion of Na+, Cl-, K+, and water.

• Effects:

• Strong, short-acting diuretic, suitable for patients with heart failure.

• Dilates renal vessels, increases renal blood flow, increases glomerular filtration rate.

• Antagonizes ADH in the distal convoluted tubule.

• Dilates veins, reduces pulmonary congestion, reduces left ventricular pressure.

• Reduces Ca++ in the blood.

# 2. Renin-Angiotensin-Aldosterone System (RAAS) Modulators

• Mechanism: Inhibit renin secretion, angiotensin II synthesis, or block the effects of angiotensin II.

• Drug groups:

• Renin inhibitors (aliskiren): Bind to the RAS at the activation site, reducing the level of renin activity in plasma.

• Angiotensin-converting enzyme (ACE) inhibitors:

• Mechanism: Inhibit angiotensin-converting enzyme, reducing the production of angiotensin II.

• Groups: Sulfhydryl group (captopril), dicarboxyl group (enalapril), phosphorus group (forsinopril).

• Effects: Vasodilation, blood pressure lowering.

• Angiotensin II type 1 receptor (AT1) blockers (ARBs): Bind to the AT1 receptor, preventing angiotensin II from binding, rendering it ineffective.

# 3. Calcium Channel Blockers

• Mechanism: Inhibit the influx of calcium into vascular smooth muscle cells and cardiomyocytes, reducing smooth muscle contraction, decreasing heart rate and left ventricular contractility, and reducing impulse conduction.

• Classification:

• Verapamil and diltiazem: Inhibit calcium influx into cardiomyocytes, reducing myocardial contractility, reducing atrioventricular conduction, slowing heart rate.

• Dihydropyridine group: Primarily act on blood vessels, without significant effects on the heart.

• Effects: Reduced myocardial contractility, vasodilation, blood pressure lowering.

• Advantages: Do not increase plasma renin activity, do not cause fluid and sodium retention, may cause increased sodium excretion, do not affect lipid and glucose metabolism.

# 4. Cardiac Glycosides

• Mechanism: Increase myocardial contractility, making the heart beat stronger, slower, and more regularly.

• Typical drugs: Digitalis, digoxin.

• Mechanism of action:

• Bind to Na+-K+ ATPase and inhibit this enzyme.

• On the kidney: Increase salt and water excretion, causing diuresis.

• On smooth muscle: Increase the contraction of gastrointestinal smooth muscle, potentially causing nausea and diarrhea.

• On the central nervous system: Stimulate the vomiting center.

Note: This article provides general information about the mechanisms of action of antihypertensive drugs on cardiac output. Consult your doctor before using any medications.