What is the common adverse effect of ACE inhibitors?

October 13, 2025 •

4 min read

Angiotensin-converting enzyme (ACE) inhibitors are widely prescribed, with over 35% of U.S. antihypertensive prescriptions being for these drugs [1.6.5]. When considering what is the common adverse effect of ACE inhibitors, a persistent dry cough is the most frequently reported issue [1.2.1, 1.2.3, 1.2.4].

Quick Summary

The most common adverse effect of ACE inhibitors is a dry, persistent cough, affecting up to 35% of patients. Other effects include dizziness, hypotension, and high potassium levels. A rare but serious side effect is angioedema.

Key Points

Dry Cough: The single most common adverse effect of ACE inhibitors is a persistent, dry cough, affecting up to 35% of users due to bradykinin accumulation [1.3.1, 1.2.2].
Bradykinin Mechanism: The cough and the rare side effect angioedema are primarily caused by the buildup of bradykinin, which is normally degraded by the ACE enzyme [1.3.1, 1.6.1].
Other Common Effects: Dizziness, hypotension (low blood pressure), and hyperkalemia (high potassium) are also common adverse effects [1.2.2, 1.2.3].
Angioedema Risk: Angioedema, a rapid swelling of the face, lips, and throat, is a rare but life-threatening emergency that can occur at any time during treatment [1.6.5, 1.6.6].
Management: The definitive treatment for ACE inhibitor-induced cough is discontinuing the medication, often switching to an Angiotensin II Receptor Blocker (ARB) [1.3.1, 1.4.2].
ACE vs. ARB: ARBs have a similar efficacy to ACE inhibitors but are much less likely to cause cough because they do not affect bradykinin levels [1.5.2, 1.5.3].
Monitoring is Key: Patients starting on ACE inhibitors require monitoring of blood pressure, potassium levels, and renal function to manage potential side effects [1.2.2].

Understanding ACE Inhibitors and Their Role

Angiotensin-converting enzyme (ACE) inhibitors are a cornerstone in the management of cardiovascular diseases, primarily hypertension (high blood pressure) and heart failure [1.2.3]. Medications in this class, such as lisinopril, enalapril, and ramipril, work by blocking the angiotensin-converting enzyme. This enzyme is a key component of the renin-angiotensin-aldosterone system (RAAS). By inhibiting this enzyme, ACE inhibitors prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. The result is vasodilation (widening of blood vessels), reduced aldosterone secretion, and consequently, lower blood pressure and reduced cardiac workload [1.2.2]. Their effectiveness in reducing cardiovascular events and mortality makes them a first-line treatment for many patients [1.7.1, 1.7.3].

The Most Common Adverse Effect: A Persistent Dry Cough

The most well-known and common adverse effect associated with ACE inhibitors is a dry, non-productive, and often tickly or scratchy cough [1.4.2, 1.2.4]. The incidence of this cough varies widely in studies, reported to affect anywhere from 5% to 35% of patients taking the medication [1.3.1]. This side effect is considered a class effect, meaning it can occur with any drug in the ACE inhibitor family [1.2.4]. The cough can begin within hours of the first dose or may not appear for weeks or even months after starting therapy [1.3.1].

Why Does the Cough Occur?

The leading theory behind the ACE inhibitor-induced cough involves the accumulation of inflammatory mediators, primarily bradykinin and substance P [1.3.1, 1.4.2]. The ACE enzyme is not only responsible for producing angiotensin II but also for breaking down bradykinin. When the enzyme is inhibited, bradykinin levels increase in the respiratory tract [1.3.3]. This accumulation can sensitize airway sensory nerves and promote bronchoconstriction, triggering the cough reflex [1.3.1, 1.3.6].

Other Common and Less Common Side Effects

While the cough is most frequent, patients may experience other adverse effects:

Hypotension and Dizziness: Especially after the first dose, a drop in blood pressure can cause dizziness or lightheadedness [1.2.2, 1.2.6]. This is more likely in patients who are dehydrated or on diuretics [1.2.3, 1.4.4]. Taking the first dose at bedtime or standing up slowly can help mitigate these symptoms [1.4.3].
Hyperkalemia (High Potassium): By reducing aldosterone secretion, ACE inhibitors decrease the excretion of potassium. This can lead to elevated potassium levels in the blood, which is a concern particularly for patients with kidney disease or those taking potassium supplements or potassium-sparing diuretics [1.2.2, 1.2.3]. Regular monitoring of potassium levels is often recommended [1.2.2].
Renal Dysfunction: In some patients, particularly those with pre-existing bilateral renal artery stenosis or severe heart failure, ACE inhibitors can lead to a decline in kidney function [1.2.3, 1.2.6]. Monitoring of serum creatinine levels is crucial, especially when initiating therapy [1.2.2].
Taste Disturbances (Dysgeusia): Some individuals report a loss of taste or a metallic taste in their mouth [1.2.1].

Serious but Rare Adverse Effect: Angioedema

A much less common but potentially life-threatening adverse effect of ACE inhibitors is angioedema [1.6.3]. It occurs in about 0.1% to 0.7% of patients [1.6.5]. Angioedema is a rapid, non-pitting swelling of the deeper layers of the skin and mucous membranes [1.6.2]. It most often affects the lips, tongue, face, and upper airway [1.6.5].

Like the cough, angioedema is also believed to be a bradykinin-mediated event [1.6.1]. Swelling of the larynx can lead to airway obstruction and asphyxiation, making it a medical emergency [1.6.4, 1.6.6]. This reaction can occur at any point during treatment, even years after a patient has been taking the medication without issue [1.6.2]. Due to the risk, a history of ACE inhibitor-induced angioedema is a contraindication to using any drug from this class again [1.6.6].

Comparison Table: ACE Inhibitors vs. Angiotensin II Receptor Blockers (ARBs)

ARBs are another class of medication that acts on the RAAS but through a different mechanism. They are often used as an alternative for patients who cannot tolerate ACE inhibitors [1.4.2].


Feature	ACE Inhibitors	Angiotensin II Receptor Blockers (ARBs)
Mechanism	Inhibit ACE enzyme, blocking Angiotensin II formation and increasing bradykinin [1.5.5].	Directly block Angiotensin II from binding to its AT1 receptor; do not affect bradykinin [1.5.5].
Cough	Common (5-35% incidence) [1.3.1].	Much lower risk; similar to placebo [1.5.2, 1.5.3].
Angioedema	Higher risk (0.1-0.7%) [1.6.5].	Lower risk, but can still occur in patients with a history of ACE inhibitor angioedema [1.5.1, 1.5.4].
Efficacy	Generally considered equivalent for blood pressure control and cardiovascular outcomes [1.5.2, 1.5.6].	Generally considered equivalent for blood pressure control and cardiovascular outcomes [1.5.2, 1.5.6].
Tolerability	Overall withdrawal rates due to side effects are higher [1.5.2].	Better tolerated, largely due to the lower incidence of cough [1.5.3, 1.5.4].

Managing Adverse Effects

If a patient develops a bothersome cough, the most effective solution is to discontinue the ACE inhibitor [1.3.1]. The cough typically resolves within 1 to 4 weeks after stopping the medication, though it can sometimes linger for up to three months [1.9.2]. In some cases of mild cough, a physician may recommend continuing the medication, as the cough can sometimes resolve on its own over several months [1.9.4]. However, for most, a switch to an ARB is the standard approach [1.4.2]. For dizziness or hypotension, adjusting the dose or the timing of administration can be effective [1.4.3]. Any signs of angioedema, such as swelling of the lips or tongue, require immediate medical attention [1.8.1].

Conclusion

While ACE inhibitors are highly effective medications for hypertension and heart failure, they are associated with several key adverse effects. The most common is a persistent, dry cough, driven by the accumulation of bradykinin. Other notable side effects include dizziness, high potassium levels, and, rarely, life-threatening angioedema. Understanding these potential effects allows patients and clinicians to monitor for issues and make informed decisions about treatment, such as switching to an alternative like an ARB if side effects become intolerable.

For more in-depth information, you can visit the National Center for Biotechnology Information (NCBI) bookshelf on ACE Inhibitors.

Frequently Asked Questions

An ACE inhibitor cough is typically a dry, persistent, and tickly or scratchy cough that does not produce phlegm. It can be bothersome and may interfere with sleep or speaking [1.4.2, 1.4.5].

The cough can start within hours of taking the first dose or may be delayed, appearing weeks or even months after initiating therapy [1.3.1].

In some cases, a mild cough may improve or disappear over time with continued use [1.9.3, 1.9.4]. However, for most people with a bothersome cough, the only effective treatment is to stop taking the medication [1.3.1].

After discontinuing the ACE inhibitor, the cough usually resolves within one to four weeks. In some cases, it may take up to three months to fully disappear [1.9.2].

No, the cough is a class effect, meaning it is common to all ACE inhibitors. Switching to a different ACE inhibitor is unlikely to resolve the cough [1.2.4].

Angioedema is a rapid swelling of the deep layers of skin, often affecting the lips, tongue, and throat. It is dangerous because if the swelling affects the airway, it can cause difficulty breathing and become life-threatening. It requires immediate medical attention [1.6.3, 1.6.4, 1.8.1].

A common alternative is an Angiotensin II Receptor Blocker (ARB), such as losartan or valsartan. ARBs work in a similar way to lower blood pressure but have a much lower risk of causing a cough [1.4.2, 1.5.3].