Prescribing Safety Assessment (PSA) 2025 – 400 Free Practice Questions to Pass the Exam

ACE inhibitors are primarily known for their role in inhibiting the angiotensin-converting enzyme, which leads to a decrease in the production of angiotensin II. Angiotensin II is a potent stimulator of aldosterone secretion from the adrenal cortex. By inhibiting the formation of angiotensin II, ACE inhibitors lead to reduced levels of aldosterone in the body. Aldosterone is a hormone that promotes sodium reabsorption and potassium excretion in the kidneys.

When aldosterone levels decrease due to the action of ACE inhibitors, this results in decreased sodium reabsorption and less potassium being excreted. As a consequence, potassium levels in the blood can rise, leading to hyperkalemia. Thus, the mechanism through which ACE inhibitors cause hyperkalemia is the reduced production of aldosterone, resulting in less potassium excretion by the kidneys.

The other options presented do not correctly convey the mechanism of action for ACE inhibitors in relation to hyperkalemia. For instance, increasing aldosterone production would lead to greater potassium excretion, not retention, while inhibiting sodium reabsorption directly does not explain the rise in potassium levels. Additionally, increased potassium excretion is the opposite effect seen with ACE inhibitor usage.