A patient is prescribed an ACE Inhibitor after experiencing a myocardial infarction. What therapeutic effects will this medication achieve?

ACE inhibitors — such as lisinopril, enalapril, and ramipril — block the angiotensin-converting enzyme, which normally converts angiotensin I to the potent vasoconstrictor angiotensin II. Without angiotensin II, aldosterone secretion is also reduced. Aldosterone normally acts on the renal collecting duct to retain sodium and water while excreting potassium. By blocking this pathway, ACE inhibitors cause the kidneys to excrete sodium and water, reducing preload, afterload, and blood pressure. After a myocardial infarction, ACE inhibitors are prescribed to reduce cardiac workload, prevent adverse ventricular remodeling, and improve long-term survival. The therapeutic effect being targeted in this question is the excretion of sodium and water, which reduces circulating volume and decreases the workload on the already-stressed myocardium. Vasoconstriction is the opposite of what ACE inhibitors do — they cause vasodilation by reducing angiotensin II levels. Calcium excretion is not a primary mechanism of ACE inhibitors; calcium channel blockers address calcium pathways. Bradycardia is associated with beta-blockers, not ACE inhibitors; ACE inhibitors do not significantly alter heart rate as a primary therapeutic effect.