Which mechanism allows ACE inhibitors to exert their therapeutic effects?

ACE inhibitors primarily exert their therapeutic effects by preventing the breakdown of bradykinin. This is significant because bradykinin is a peptide that causes blood vessels to dilate, leading to lower blood pressure. By inhibiting the enzyme angiotensin-converting enzyme (ACE), these medications increase bradykinin levels, resulting in vasodilation and improved blood flow. This mechanism ultimately contributes to the antihypertensive effects that make ACE inhibitors effective in treating conditions such as hypertension and heart failure.

The therapeutic benefit of ACE inhibitors also stems from their ability to reduce the production of angiotensin II, a potent vasoconstrictor. However, the therapeutic action is largely attributed to the elevated bradykinin levels, which promote vasodilation. The balance between these opposing effects can also be a reason clinicians monitor patients on ACE inhibitors closely to assess both their blood pressure management and potential side effects related to bradykinin, such as cough or angioedema.