What do ACE inhibitors, ARBs, and thiazide diuretics decrease in terms of cardiovascular function?

ACE inhibitors, Angiotensin Receptor Blockers (ARBs), and thiazide diuretics play significant roles in managing hypertension and heart failure by impacting the hemodynamics of the cardiovascular system.

These agents reduce both preload and afterload, which contributes to their effectiveness in lowering blood pressure and improving heart function.

ACE inhibitors and ARBs primarily act by blocking the renin-angiotensin-aldosterone system (RAAS). By inhibiting angiotensin II formation or blocking its effects, these medications lead to vasodilation, thereby reducing afterload—the resistance the heart must pump against to circulate blood. Moreover, they can decrease fluid retention by reducing aldosterone production, which decreases blood volume and consequently preload.

Thiazide diuretics assist by promoting diuresis, leading to a reduction of extracellular fluid volume. This decrease in volume lowers preload, or the amount of blood returning to the heart, while also causing some vasodilatory effects that can help in decreasing afterload.

Through these mechanisms, ACE inhibitors, ARBs, and thiazide diuretics collectively reduce the workload on the heart, facilitate better cardiac output, and decrease the risk of cardiovascular events associated with high blood pressure.