Do ACE inhibitors cause coughing? The surprising side effect explained

October 11, 2025 •

3 min read

ACE inhibitors can cause a persistent dry cough in approximately 5% to 35% of patients, a well-documented side effect that is often a primary reason for discontinuing the medication. While effective for managing conditions like high blood pressure and heart failure, the distinctive cough can significantly impact a patient's quality of life.

Quick Summary

A persistent, dry, and non-productive cough is a recognized side effect of ACE inhibitors. It is caused by the accumulation of bradykinin in the airways, a substance that is normally broken down by the ACE enzyme. The cough is not dose-dependent and typically resolves after discontinuing the medication. Alternative drug classes, such as ARBs, can be used for patients who experience this adverse effect.

Key Points

Dry, persistent cough: ACE inhibitor cough is typically dry, tickly, and non-productive, differing from a cough caused by infection.
Bradykinin accumulation: The underlying mechanism involves the build-up of bradykinin and substance P in the airways due to ACE inhibition, irritating the cough reflex.
Common but not universal: The incidence of cough varies widely, affecting a significant portion of users, but not everyone on the medication will experience it.
Resolution after discontinuation: The cough usually resolves within 1 to 4 weeks after stopping the ACE inhibitor, though it can take up to three months.
Effective alternatives exist: Angiotensin II Receptor Blockers (ARBs) are a primary alternative, offering similar therapeutic benefits with a much lower risk of causing a cough.
Consult your doctor: Patients should never stop their ACE inhibitor abruptly and should always consult their healthcare provider for guidance on managing the cough.

Understanding the Link Between ACE Inhibitors and Cough

Angiotensin-converting enzyme (ACE) inhibitors are a class of medications widely used to treat cardiovascular conditions such as high blood pressure (hypertension), heart failure, and chronic kidney disease. Common examples include lisinopril, enalapril, and ramipril, often identified by the '-pril' suffix. These drugs are highly effective in blocking a crucial step in the body's renin-angiotensin-aldosterone system (RAAS), which helps to relax blood vessels and lower blood pressure.

However, a notable and sometimes bothersome side effect of this medication class is a persistent, dry cough. While the cough is generally not a sign of a serious condition, its persistent and irritating nature can affect a patient's daily life and lead them to stop their medication without consulting a doctor. It is important to recognize that this is a recognized adverse effect of the drug class, and effective management strategies are available.

Why Do ACE Inhibitors Cause a Cough? The Bradykinin Connection

The most widely accepted theory behind the ACE inhibitor-induced cough involves the chemical bradykinin. The ACE enzyme has another function besides its role in blood pressure regulation: it breaks down certain substances in the body, including bradykinin and substance P. When an ACE inhibitor blocks the ACE enzyme, it prevents the breakdown of these substances, causing them to accumulate in the respiratory system.

Here is a simple breakdown of the mechanism:

ACE inhibitors block the ACE enzyme. This stops the conversion of angiotensin I to angiotensin II, leading to lower blood pressure.
Bradykinin levels rise. Since the ACE enzyme degrades bradykinin, its inhibition increases bradykinin concentration.
Airway irritation. Elevated bradykinin and substance P in the airways cause inflammation and stimulate sensory nerves.
Triggered cough reflex. The stimulation of these nerves, particularly the C-fibers, triggers a persistent, non-productive cough.

What Kind of Cough Is It?

An ACE inhibitor cough is typically a persistent, dry, and non-productive cough, unlike an infection-related cough. It doesn't produce mucus and is often described as a tickling or scratching sensation in the throat. The cough can begin hours or months after starting the medication.

How Common is an ACE Inhibitor Cough?

The incidence of ACE inhibitor cough ranges from approximately 5% to 35% of patients. It is one of the main reasons patients discontinue ACE inhibitor therapy.

Risk factors for developing the cough include:

Female gender.
Older age (over 65).
Non-smokers.
Asian descent.

Managing an ACE Inhibitor Cough

If a cough develops while on an ACE inhibitor, do not stop the medication without consulting a healthcare provider, as abrupt discontinuation can cause blood pressure to rise. The cough usually stops within a few weeks of discontinuing the medication.

Management strategies your doctor might consider include:

Switching to an ARB: Angiotensin II Receptor Blockers (ARBs) are a common and effective alternative. They block angiotensin II receptors without affecting bradykinin levels, significantly lowering the risk of cough.
Switching to a different ACE inhibitor: This may not be successful as cough is a class effect, and recurrence is possible.
Combination therapy: Adding a calcium channel blocker or diuretic might help alleviate the cough while continuing the ACE inhibitor.
Other pharmacological options: In some cases, medications like cromolyn or theophylline might reduce the cough, but these are not for routine use.

Comparison of Treatment Options for ACE Inhibitor Cough


Option	Mechanism of Action	Effectiveness for Cough	Risk of Cough	Notes
Switch to ARB	Blocks Angiotensin II receptors, bypasses bradykinin pathway	Highly effective; resolves cough in most patients	Very low risk (comparable to placebo)	Recommended first-line alternative
Stay on ACE Inhibitor	Continues ACE inhibition, bradykinin remains elevated	Ineffective; cough persists	High risk in susceptible individuals	Consider only if cough is mild and tolerable; not recommended if bothersome
Add Calcium Channel Blocker	May inhibit prostaglandin synthesis	Variable; may reduce severity in some cases	Moderate risk, but lower than monotherapy	Combination therapy, requires doctor's supervision
Switch to another ACE Inhibitor	Same mechanism, relies on different tissue affinity	Limited success; cough can recur	Varies by drug, but overall high risk	Not a recommended strategy for managing cough

Conclusion

In summary, ACE inhibitors can cause a persistent, dry cough in a significant number of patients due to bradykinin accumulation. This side effect often leads to discontinuation of the medication. ARBs are effective alternatives that offer similar cardiovascular benefits with a much lower risk of cough. Patients experiencing this cough should consult their doctor to find a suitable treatment plan.

For more clinical information, see the CHEST Journal article on ACE inhibitor-induced cough.

Frequently Asked Questions

The cough is primarily caused by the accumulation of bradykinin and substance P in the lungs and airways. The ACE enzyme, which is inhibited by the medication, normally breaks down these substances.

The onset of the cough can vary widely. It may occur within hours of the first dose, or it could take weeks or months to develop after starting treatment.

No, the cough is not dependent on the dose of the ACE inhibitor. It is an idiosyncratic reaction, meaning it occurs in susceptible individuals regardless of the dosage.

The cough is typically described as a dry, persistent, and hacking cough, often accompanied by a tickle or scratchy feeling in the throat.

The most common and effective alternative is to switch to an Angiotensin II Receptor Blocker (ARB), such as losartan or valsartan. Other options may include a different class of blood pressure medication.

Switching to a different ACE inhibitor is not generally recommended because the cough is considered a class effect. There is a high chance the cough will recur with another drug in the same class.

The cough typically resolves within 1 to 4 weeks after discontinuing the ACE inhibitor. In some cases, it can linger for up to three months.