ARB vs ACE Inhibitor: How They Differ and Which One Is Right for You

A 58-year-old woman comes to clinic with a blood pressure of 152/94 and a recent diagnosis of type 2 diabetes. Her primary doctor started her on lisinopril a few weeks ago. The blood pressure is better, but she's been waking up at night with a dry, tickly cough that won't quit. She's tried lozenges, more water, sleeping propped up. Nothing helps. She wants to know if the medication is the cause and what we can do about it. We switch her to losartan, an angiotensin receptor blocker. Within ten days the cough is gone, her blood pressure stays controlled, and she's sleeping through the night again.

I'm Dr. Damian Rasch, a cardiologist in Encinitas. Patients ask me about ACE inhibitors and ARBs almost every week, usually some version of "are these the same drug" or "why did my doctor switch me." They aren't the same, but they hit the same biological target from different angles, and for most people the choice between them comes down to side effects and a few specific clinical situations. This article walks through how each class works, when I reach for one over the other, what the side effects look like in real life, and how to think about the dozen or so options inside each class.

How ACE Inhibitors Work

To understand ACE inhibitors, you need a one-minute version of the renin-angiotensin-aldosterone system, or RAAS. Your kidneys release a hormone called renin when they sense low blood pressure or low blood volume. Renin starts a cascade. It converts a precursor protein into angiotensin I, and then an enzyme called angiotensin-converting enzyme (ACE for short) converts angiotensin I into angiotensin II. Angiotensin II is the active hormone, and it does several things. It clamps down on blood vessels (raising blood pressure), tells the adrenal glands to release aldosterone (causing the kidneys to retain salt and water), and drives long-term remodeling of the heart and blood vessels in ways that aren't healthy if the system is chronically activated.

ACE inhibitors block the converting enzyme. Less angiotensin II gets made. Blood vessels relax, the kidneys hold onto less salt and water, and over time the heart and blood vessels remodel in a healthier direction. Blood pressure comes down. In patients with heart failure, the heart works against less resistance and has more time to recover function. In patients with diabetes and protein in the urine, the kidneys are protected from the long-term damage that high pressure inside the kidney filters causes.

The names are easy to spot once you know the pattern. They almost all end in "pril." Lisinopril, ramipril, enalapril, benazepril, captopril, fosinopril, quinapril, perindopril, trandolapril. They have small differences in dosing, half-life, and how the kidneys and liver handle them, but they work through the same mechanism.

How ARBs Work

ARBs (angiotensin receptor blockers) take a different approach to the same problem. Instead of blocking the enzyme that makes angiotensin II, they block the receptor that angiotensin II binds to. Angiotensin II still gets made in normal quantities, but it can't dock onto its main receptor (the AT1 receptor), so it can't deliver its message. The downstream effects are similar to what ACE inhibitors produce. Blood vessels relax, salt and water get released, and the long-term remodeling improves.

The names of ARBs end in "sartan." Losartan, valsartan, olmesartan, irbesartan, telmisartan, candesartan, azilsartan, eprosartan. As with ACE inhibitors, the individual drugs have differences in half-life, potency, and how the body clears them, but the mechanism is shared.

The practical question patients often ask is "if they do the same thing, why do we have both classes." The answer is in the details of how the two classes differ at the level of side effects and a few specific outcomes. ACE inhibitors block ACE itself, and ACE has other jobs in the body besides making angiotensin II. One of those jobs is breaking down a peptide called bradykinin. When ACE is blocked, bradykinin builds up, and that buildup is what drives the dry cough some patients get on ACE inhibitors. It also drives a rare but serious problem called angioedema, where parts of the face, lips, tongue, or airway swell up. ARBs don't touch ACE, so they don't cause bradykinin buildup, and they don't cause cough or angioedema at the same rates.

Why We Have Both Classes

ACE inhibitors came first, in the late 1970s and 1980s, with captopril and then enalapril leading the way. The trials that established their value in heart failure (CONSENSUS and SOLVD) and after heart attacks (SAVE, AIRE) and in diabetic kidney disease (Lewis trial of captopril) were practice-changing. For about a decade, ACE inhibitors were the default RAAS blocker for almost every cardiovascular indication.

The cough was the problem. Estimates vary, but somewhere between 5 and 20 percent of patients on ACE inhibitors develop a persistent dry cough. In some populations the rate is higher. Once the cough starts, it doesn't go away with continued use. Patients stop taking the drug, or they suffer through it, or their doctor switches them. ARBs were developed to provide RAAS blockade without the bradykinin-driven side effects, and losartan came to market in 1995 as the first agent in the class. Subsequent trials (LIFE, VALUE, ONTARGET, CHARM) established that ARBs were as effective as ACE inhibitors for most indications, with a much better tolerability profile.

So why do we still use ACE inhibitors at all? A few reasons. They've been around longer, they're inexpensive, the cardiovascular evidence base is enormous, and for many patients they work fine without causing cough. In some specific situations (post-myocardial infarction, certain heart failure scenarios with strong historical data), I still reach for an ACE inhibitor first. But for a patient starting RAAS blockade today with no compelling reason to pick one over the other, an ARB is often the more comfortable choice.

When ACE Inhibitors Are First-Line

There are a few clinical situations where the trial data is strongest for an ACE inhibitor and where I tend to start there.

After a heart attack, especially one that damaged a meaningful portion of the left ventricle, ACE inhibitors reduce mortality and prevent progression to heart failure. The SAVE trial (captopril after MI) and AIRE (ramipril after MI with heart failure) showed clear mortality benefits. The HOPE trial extended this to patients with vascular disease or high-risk diabetes, where ramipril reduced cardiovascular events. For a patient I'm seeing in the weeks after a heart attack, an ACE inhibitor is usually where I start.

Heart failure with reduced ejection fraction has a long history with ACE inhibitors as foundational therapy. CONSENSUS, with enalapril in severe heart failure, was the first trial showing that any drug could reduce mortality in this population. SOLVD followed and showed similar benefits in milder heart failure. ARBs eventually entered the picture (CHARM with candesartan, VALIANT with valsartan after MI) and showed comparable benefits. Today the conversation has shifted again with ARNI therapy (sacubitril-valsartan, brand name Entresto), which I'll get to.

Diabetic kidney disease with protein in the urine is another situation where ACE inhibitors have strong evidence. The Lewis trial with captopril in type 1 diabetes showed reduced progression to end-stage kidney disease. Trials with ARBs (RENAAL with losartan, IDNT with irbesartan) showed similar benefits in type 2 diabetes. Either class is appropriate; ACE inhibitors are often started first because of cost and history, but if the patient has cough, switching to an ARB preserves the kidney protection.

When ARBs Are First-Line

The clearest indication for starting with an ARB is intolerance to ACE inhibitors. If a patient has had cough or angioedema on an ACE inhibitor, the ARB is the right choice. The cough resolves within a week or two of switching in nearly every patient I've treated. The angioedema risk is lower with ARBs (probably under 1 percent and likely closer to 0.1 percent) compared with ACE inhibitors, although it's not zero.

For Black patients, both ACE inhibitors and ARBs work, but the blood pressure response is sometimes blunted compared with calcium channel blockers or thiazide diuretics when used as monotherapy. The ALLHAT trial and others informed this. In Black patients with hypertension and no compelling indication for RAAS blockade, I often start with a calcium channel blocker or chlorthalidone, then add an ACE inhibitor or ARB if needed. In Black patients with heart failure or diabetic kidney disease, RAAS blockade is still appropriate, and ARBs are reasonable first-line.

For patients who have tolerated an ARB previously or who simply want to avoid even the small risk of cough, starting with an ARB is reasonable. The cardiovascular outcomes are comparable across most indications. The cost difference between generic ACE inhibitors and generic ARBs has narrowed substantially, so the price argument that used to favor ACE inhibitors is weaker than it was a decade ago.

Are They Interchangeable for Hypertension

For garden-variety hypertension without compelling indications, ACE inhibitors and ARBs are largely interchangeable. Both lower blood pressure by similar amounts at equivalent doses. Both reduce cardiovascular events over time. The trial that most directly compared them in a high-risk population was ONTARGET, which randomized patients with vascular disease or high-risk diabetes to ramipril, telmisartan, or both. The two single-agent arms had nearly identical outcomes. The combination arm had more side effects (kidney injury, hyperkalemia, hypotension) without better outcomes, which is the trial that put the nail in the coffin of routine ACE-I plus ARB combination therapy.

In clinic, when I'm starting RAAS blockade for hypertension, I think about a few things. Has the patient had any prior reaction to an ACE inhibitor? Do they have a strong family history of angioedema? Are they Black? Do they have diabetes or kidney disease that would benefit from RAAS blockade? Are they on a budget that favors the cheapest available option? The answers shape whether I pick an ACE inhibitor or an ARB, but for many patients either would work.

Heart Failure: Where Each Fits and the Role of ARNI

Heart failure with reduced ejection fraction (HFrEF, defined as EF less than or equal to 40 percent) is a setting where the conversation has evolved. For decades the foundation was an ACE inhibitor (or an ARB if intolerant), a beta-blocker, and a mineralocorticoid receptor antagonist (spironolactone or eplerenone). Then PARADIGM-HF changed the game. That trial randomized patients with HFrEF to either enalapril or sacubitril-valsartan (the latter being a combination of valsartan with sacubitril, which inhibits an enzyme that breaks down protective natriuretic peptides). Sacubitril-valsartan reduced cardiovascular death and heart failure hospitalization by about 20 percent compared with enalapril. The trial was stopped early because of the magnitude of benefit.

After PARADIGM-HF, sacubitril-valsartan (brand name Entresto) became the preferred RAAS blocker in HFrEF for patients who can tolerate it and afford it. The current AHA/ACC heart failure guidelines list ARNI as the preferred first agent in the class, with ACE inhibitors and ARBs as alternatives if ARNI isn't feasible. There's a 36-hour washout required when switching from an ACE inhibitor to ARNI to avoid stacking the angioedema risks; switching from an ARB to ARNI doesn't require a washout.

The current four-drug foundation of HFrEF therapy is ARNI (or ACE-I/ARB), a beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and an SGLT2 inhibitor (dapagliflozin or empagliflozin). Each class delivers a separate mortality benefit, and the four together represent the modern standard. For a patient with new HFrEF, my goal is to get them on all four classes at evidence-based doses as soon as their blood pressure, kidney function, and potassium tolerate it.

For heart failure with preserved ejection fraction (HFpEF), the data is different. ARBs (candesartan in CHARM-Preserved, irbesartan in I-PRESERVE) didn't show the same mortality benefit as in HFrEF. SGLT2 inhibitors are the current standout in HFpEF. RAAS blockade is reasonable for blood pressure control in HFpEF, but I don't expect the same magnitude of mortality benefit.

Common Side Effects of Each

The side effect profiles of ACE inhibitors and ARBs overlap substantially because they share a mechanism. A few side effects belong to both, a few belong mostly to ACE inhibitors, and one (angioedema) is more common with ACE inhibitors but can happen with either.

Cough

Dry, tickly cough is the classic ACE inhibitor side effect. It's caused by bradykinin and substance P accumulating in the airways. The cough can start within days of starting the drug or appear weeks to months later. It doesn't get better with cough syrups, antihistamines, or inhalers because the cause isn't allergy or postnasal drip; it's the drug itself. The only fix is stopping the medication, after which the cough usually resolves within a week or two. ARBs cause cough at rates close to placebo, so switching from an ACE inhibitor to an ARB resolves the cough in nearly all patients.

Angioedema

Angioedema is rapid swelling of the face, lips, tongue, or airway. It's rare (around 0.3 percent with ACE inhibitors, much lower with ARBs), but it can be life-threatening when it involves the airway. The risk is higher in Black patients and in patients with prior angioedema from any cause. If a patient has angioedema on an ACE inhibitor, I generally avoid ARBs as well unless the situation is compelling, because there's some cross-reactivity. Patients who develop angioedema need to know never to take an ACE inhibitor again, and they need an emergency plan if symptoms recur.

Hyperkalemia

Both classes can raise serum potassium. The mechanism is reduced aldosterone, which reduces potassium excretion in the kidney. Mild rises in potassium are common and usually clinically irrelevant. Significant hyperkalemia (over 5.5 mEq/L) is more likely in patients with reduced kidney function, in patients on potassium supplements or potassium-sparing diuretics (spironolactone, eplerenone), in patients with diabetes, and in older adults. Routine monitoring of basic metabolic panel a couple of weeks after starting and periodically thereafter is standard practice. If potassium climbs too high, the dose may need to come down or the drug may need to be stopped.

Kidney Function Changes

Both classes can cause a small rise in serum creatinine after initiation, often around 10 to 20 percent. A rise in that range is expected and reflects the medication doing what it's supposed to do (reducing pressure inside the kidney filters). It doesn't mean the kidneys are being damaged. A rise of more than 30 percent should prompt evaluation for renal artery stenosis, volume depletion, or other reversible causes, and may warrant stopping the drug. In patients with significant chronic kidney disease, both classes can still be used and often should be, because the long-term kidney protection outweighs the early creatinine bump in most cases.

Hypotension

Both classes lower blood pressure, and in volume-depleted patients (those on high-dose diuretics, with vomiting or diarrhea, or with very tight blood pressure control already) the first dose can drop pressure more than expected. Starting low and titrating up, holding doses on sick days, and being attentive to volume status mitigate this. Patients with bilateral renal artery stenosis can have steep blood pressure drops with RAAS blockade, which is one reason to avoid these drugs in that setting.

Pregnancy

Both ACE inhibitors and ARBs are contraindicated in pregnancy. Use during pregnancy can cause fetal kidney damage, low amniotic fluid, and birth defects. Women of childbearing age on either class need reliable contraception or need to switch to a pregnancy-safe alternative when planning conception or as soon as pregnancy is suspected.

Combining ACE Inhibitor and ARB

A reasonable instinct, on first thought, is that if blocking RAAS at the enzyme step is good and blocking it at the receptor is good, blocking it at both should be better. The instinct is wrong. ONTARGET, which compared ramipril, telmisartan, and the combination in high-risk patients, showed that the combination produced more side effects (kidney injury, hyperkalemia, hypotension, syncope) without better cardiovascular outcomes. VA NEPHRON-D, in patients with diabetic kidney disease, was stopped early for safety concerns with combination therapy. The general rule now is don't combine an ACE inhibitor with an ARB.

There are a few rare exceptions in specialized hands. Some heart failure programs have used dual RAAS blockade in highly selected patients. Some kidney specialists use it in proteinuric kidney disease in selected patients with very close monitoring. These are exceptions to the rule, and they require ongoing close oversight. For most patients in most settings, pick one or the other.

Sacubitril-valsartan (ARNI) contains an ARB but isn't an ACE inhibitor, so it can be combined with most other heart failure medications. It can't be combined with an ACE inhibitor (with a 36-hour washout required between them) because of additive angioedema risk.

Drug Selection Within Each Class

Once I've decided whether the patient gets an ACE inhibitor or an ARB, I have to pick a specific drug. The choice depends on the indication, dosing convenience, kidney function, and what's been studied in the trial that drives the decision.

ACE Inhibitor Choices

Lisinopril is my workhorse for hypertension. It's once-daily, generic, inexpensive, well-tolerated, and the dose range (5 to 40 mg) covers most patients. It's not the active form of the drug but doesn't require liver activation, so it's a good choice in patients with liver disease.

Ramipril is what I use when I want to invoke the HOPE trial data (vascular disease or high-risk diabetes patients without heart failure). It's once-daily and generic. The HOPE evidence is strong enough that I'll often choose ramipril over lisinopril when the patient fits the HOPE population.

Enalapril has the deepest heart failure evidence (CONSENSUS, SOLVD, and the comparator arm of PARADIGM-HF). It's twice-daily, which is a downside for adherence, but for patients with heart failure who aren't candidates for ARNI, enalapril is a reasonable choice with a long track record.

Captopril is rarely used for chronic therapy now because it's three-times-daily dosing, but it has historical importance and is sometimes used in specific situations like the early hours after MI when short half-life is useful.

Benazepril, fosinopril, quinapril, perindopril, and trandolapril all exist and are used in various settings. Differences between them are minor for most patients.

ARB Choices

Losartan is the original ARB, generic, inexpensive, and effective. The LIFE trial established its benefit in hypertension with left ventricular hypertrophy, and RENAAL established its benefit in diabetic kidney disease. It's a reasonable starting ARB for many patients.

Valsartan has strong evidence in heart failure (Val-HeFT, VALIANT after MI) and is the ARB component of sacubitril-valsartan. For patients with HFrEF who can't tolerate ARNI but need an ARB, valsartan has the strongest data.

Olmesartan is a potent ARB with strong blood pressure lowering effects. There was a concern years back about a sprue-like enteropathy (severe diarrhea and weight loss) with olmesartan, which is rare but real, so if a patient on olmesartan develops unexplained chronic diarrhea, the drug is on my list to consider.

Irbesartan has strong evidence in diabetic kidney disease (IDNT). Telmisartan has the longest half-life of any ARB and the ONTARGET data showing equivalence to ramipril for cardiovascular outcomes. Candesartan has the CHARM trial data in heart failure. Azilsartan is one of the newer ARBs with potent blood pressure lowering, branded and more expensive than the older generics.

Common Patient Questions

Will an ARB make my cough go away?

If your cough started after you began an ACE inhibitor and has no other clear cause, switching to an ARB usually resolves it within a week or two. The cough is caused by bradykinin buildup, which is specific to ACE inhibitors. ARBs don't cause that buildup. If your cough doesn't resolve after switching, something else is driving it (postnasal drip, asthma, GERD, infection), and that needs separate evaluation.

Are ARBs safer than ACE inhibitors?

"Safer" depends on what you mean. ARBs cause cough less often, cause angioedema less often, and tend to be slightly better tolerated. The serious side effects that both classes share (kidney function changes, hyperkalemia, low blood pressure) happen at similar rates with both. Both have the same pregnancy risks. So in terms of overall tolerability, ARBs win modestly. In terms of catastrophic side effects, the two classes are comparable, with ARBs having a small advantage on angioedema risk.

Why am I on a "pril" if I have heart failure when ARBs are easier to tolerate?

For decades, the heart failure trial data was strongest with ACE inhibitors, and many patients were started on them based on that history. The current guidelines favor ARNI (sacubitril-valsartan) when feasible, but if cost or insurance is a barrier, an ACE inhibitor is still a reasonable choice with strong evidence. If you're tolerating it without cough or other side effects, there's no urgent reason to switch. If you have any side effects, talk with your cardiologist about transitioning to an ARB or ARNI.

Can I take an ACE inhibitor or ARB with my potassium supplement?

Both classes raise potassium, and adding a potassium supplement on top of that can push potassium dangerously high. If you've been told to take potassium for any reason, your prescriber needs to know you're on a RAAS blocker so the potassium dose can be adjusted or the supplement reconsidered. Same goes for potassium-sparing diuretics like spironolactone or eplerenone, which raise potassium even more. Routine blood work catches problems before they become serious, but only if you're getting the labs done.

My creatinine went up after I started this medication. Should I stop?

Not necessarily. A small rise (10 to 20 percent) is expected and reflects the medication working as intended on the kidney filters. The long-term effect, especially in patients with diabetes or kidney disease, is kidney protection. A larger rise (over 30 percent) needs evaluation, and the drug may need to be paused or reduced. Don't stop on your own; check with your prescriber, who can decide whether the change is expected or warrants action.

Do I need to take this for the rest of my life?

For most chronic indications, yes, you do. Hypertension, heart failure, and diabetic kidney disease are long-term conditions, and the benefit of RAAS blockade depends on continued use. Stopping the medication causes blood pressure to rise and the underlying disease processes to progress. The exception is short-term post-MI use in patients with normal ejection fraction and no other indication, where the duration of therapy is sometimes individualized. Most patients on these drugs are on them for life.

What should I do on a sick day with vomiting or diarrhea?

If you're significantly volume-depleted from vomiting or diarrhea, holding the medication for a day or two is reasonable, because the combination of dehydration and RAAS blockade can drop blood pressure too far and stress the kidneys. Some practices give patients a written sick-day plan listing medications to hold. If you don't have one and you're feeling lightheaded with a stomach bug, it's reasonable to skip a dose or two and call your prescriber. Resume when you're eating and drinking normally.

Is one of these drugs better for my kidneys than the other?

For most kidney indications, ACE inhibitors and ARBs are comparable. The strongest historical data in type 1 diabetes is with captopril, and the strongest historical data in type 2 diabetic kidney disease is with losartan and irbesartan. Either class is appropriate for kidney protection in most patients. The choice between them comes down to side effect tolerance more than to a meaningful difference in kidney outcomes.

When to Escalate Care

Call 911 immediately for any sudden swelling of the face, lips, tongue, or throat, or for difficulty breathing or swallowing after taking an ACE inhibitor or ARB. Angioedema can progress fast, and airway involvement is a true emergency. Stop the medication and don't take another dose until you've been seen.

Contact your prescriber the same day for severe lightheadedness or fainting, especially after starting a new medication or having a dose increased. Same-day contact is also appropriate for unexplained muscle weakness or palpitations that could reflect a high potassium level, or for an acute decline in urine output.

Schedule a clinic visit within one to two weeks for a persistent dry cough that started after beginning an ACE inhibitor, for new dizziness on standing, or for blood pressure readings that are too low or too high after starting or adjusting therapy. Routine follow-up after starting RAAS blockade typically includes a basic metabolic panel at one to two weeks to check potassium and creatinine, and a clinic visit to review tolerability.

A Final Note From Me

ACE inhibitors and ARBs are two of the most useful drug classes in cardiology. They lower blood pressure, protect the heart and kidneys over years to decades, and reduce mortality in heart failure and after heart attacks. The differences between the two classes are real but smaller than patients sometimes assume. For most indications, either class will get the job done; the choice often comes down to side effect tolerance, cost, and the specific trial evidence that applies to your situation.

If you've been started on one of these drugs and you're tolerating it without side effects, the right thing to do is stay on it. Don't stop because a friend had a bad experience or because you read something online. The benefits accrue over years of consistent use, and stopping resets the clock. If you have side effects, the right thing to do is talk to your prescriber, not to suffer through them or quit on your own. Most side effects can be managed by switching to a different drug in the same class or to a drug in a different class, and the alternatives are usually well-tolerated.

If you have heart failure and you're on an older ACE inhibitor while feeling stable, it's worth a conversation about whether ARNI (sacubitril-valsartan) would be a better choice. The trial evidence supporting ARNI is strong, and many patients who feel "fine" on an ACE inhibitor feel better on ARNI, with fewer hospitalizations. Cost is a real barrier for some, but not the only consideration. The patients who stay engaged, stay on therapy, and stay in conversation with their care team are the ones who get the most out of what we have to offer.

References

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7. CONSENSUS Trial Study Group. "Effects of Enalapril on Mortality in Severe Congestive Heart Failure: Results of the Cooperative North Scandinavian Enalapril Survival Study." New England Journal of Medicine 316, no. 23 (1987): 1429-1435.

8. SOLVD Investigators, Salim Yusuf, Bertram Pitt, Curt D. Furberg, Marvin A. Konstam, Eugene Braunwald, James E. Rouleau, et al. "Effect of Enalapril on Survival in Patients with Reduced Left Ventricular Ejection Fractions and Congestive Heart Failure." New England Journal of Medicine 325, no. 5 (1991): 293-302.

9. Whelton, Paul K., Robert M. Carey, Wilbert S. Aronow, Donald E. Casey Jr., Karen J. Collins, Cheryl Dennison Himmelfarb, Sondra M. DePalma, et al. "2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults." Journal of the American College of Cardiology 71, no. 19 (2018): e127-e248.

10. Heidenreich, Paul A., Biykem Bozkurt, David Aguilar, Larry A. Allen, Joni J. Byun, Monica M. Colvin, Anita Deswal, et al. "2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure." Journal of the American College of Cardiology 79, no. 17 (2022): e263-e421.

Published on damianrasch.com. The above information was composed by Dr. Damian Rasch, drawing on individual insight and bolstered by digital research and writing assistance. The information is for educational purposes only and does not constitute medical advice.