Cardiovascular drugs

1. Renin–angiotensin–aldosterone system agents

These medicines act at different points of the renin–angiotensin–aldosterone system to lower blood pressure, reduce cardiac workload and limit adverse cardiac and renal remodelling.

• ACE inhibitors — Block conversion of angiotensin I to II; cough and angio-oedema are the classic class effects.
• Angiotensin receptor blockers — Block the AT1 receptor directly, avoiding the bradykinin-mediated cough.
• Mineralocorticoid receptor antagonists — Aldosterone antagonists with prognostic benefit in heart failure and a hyperkalaemia risk.
• Angiotensin receptor–neprilysin inhibitors — Combined AT1 blockade and neprilysin inhibition; the ACE-inhibitor washout is the key safety point.

2. Adrenergic receptor agents

These medicines block or stimulate adrenergic receptors, changing heart rate, contractility and vascular tone.

• Beta blockers — Reduce heart rate and contractility; selectivity and intrinsic activity differ sharply across the class.
• Alpha blockers — Reduce vascular tone through alpha-1 blockade; first-dose hypotension is characteristic.
• Centrally acting antihypertensives — Reduce central sympathetic outflow; rebound hypertension on abrupt withdrawal is the classic trap.

3. Calcium channel blockers

These medicines reduce calcium entry through voltage-gated channels in vascular smooth muscle and cardiac tissue, causing vasodilation or reduced cardiac conduction depending on subclass.

• Dihydropyridine calcium channel blockers — Vascular-selective agents; peripheral oedema is the dose-limiting effect.
• Non-dihydropyridine calcium channel blockers — Rate-limiting agents acting on cardiac conduction; combination with beta blockers needs care.

4. Diuretics

These medicines increase renal sodium and water excretion at defined nephron sites, reducing fluid overload and blood pressure.

• Thiazide and thiazide-like diuretics — Distal tubule agents; hyponatraemia and hypokalaemia dominate monitoring.
• Loop diuretics — Powerful ascending-limb agents used for fluid overload; ototoxicity at high doses.
• Potassium-sparing diuretics — Distal agents that conserve potassium; hyperkalaemia is the principal risk.

5. Antithrombotic agents

These medicines reduce clot formation or dissolve existing clot by acting on platelets, the coagulation cascade or fibrin, and they carry the bleeding risk that dominates their monitoring.

• Antiplatelet agents — Reduce platelet aggregation by distinct pathways; bleeding risk governs combination use.
• Vitamin K antagonists — Warfarin and relatives; INR monitoring and interactions define their use.
• Direct oral anticoagulants — Direct factor Xa or thrombin inhibitors with fixed dosing and renal dose adjustment.
• Heparins and related parenteral anticoagulants — Antithrombin-dependent agents; heparin-induced thrombocytopenia is the key adverse effect.
• Thrombolytics — Fibrinolytic agents for time-critical occlusion; contraindications are largely bleeding-related.

6. Lipid-modifying agents

These medicines lower atherogenic lipoproteins by inhibiting synthesis, reducing absorption or increasing clearance, and are central to cardiovascular risk reduction.

• Statins — HMG-CoA reductase inhibitors; myopathy and interaction profile are the examinable points.
• Cholesterol absorption inhibitors — Reduce intestinal cholesterol absorption; commonly added to a statin.
• PCSK9 inhibitors — Monoclonal or RNA-based agents that increase LDL receptor recycling.
• Fibrates — PPAR-alpha agonists used mainly for hypertriglyceridaemia; myopathy risk with statins.

7. Antiarrhythmic agents

These medicines alter cardiac ion currents or conduction to restore or maintain rhythm, and several are themselves proarrhythmic.

• Class I antiarrhythmics (sodium channel blockers) — Sodium channel blockers subdivided by kinetics; proarrhythmia limits use.
• Class III antiarrhythmics (potassium channel blockers) — Prolong repolarisation; amiodarone toxicity is a major examinable topic.

8. Vasodilators and other cardiac agents

These medicines reduce preload or afterload, or act through mechanisms best studied separately from the main cardiovascular families.

• Nitrates — Nitric oxide donors reducing preload; tolerance and PDE5-inhibitor interaction are critical.
• Cardiac glycosides — Digoxin and relatives; narrow therapeutic index and toxicity recognition dominate.
• Sinus node and metabolic cardiac agents — Ivabradine, ranolazine and related agents acting outside the main families.

Studying this the efficient way

Learn the mechanism family first, then the classes inside it. Almost every exam question about spectrum, adverse effects or resistance is really a question about which mechanism a drug belongs to. Each class page ends with a 60-second revision block and the traps students most often fall for.

Back to the Pharmacology Study Corner · Drug Library A–Z