Losartan is a widely prescribed medication for managing high blood pressure (hypertension) and treating conditions like heart failure and diabetic kidney disease. To answer the question directly, Losartan is not an Angiotensin-Converting Enzyme (ACE) inhibitor. It belongs to a distinct class of cardiovascular drugs known as Angiotensin II Receptor Blockers (ARBs). Both classes target the same regulatory pathway in the body, but they intervene at different points, which results in differences in their clinical profiles and side effects.
Understanding Angiotensin II Receptor Blockers
Losartan, often prescribed as Losartan Potassium, is a prime example of an Angiotensin II Receptor Blocker (ARB). The drug works by targeting the Renin-Angiotensin-Aldosterone System (RAAS), a complex hormonal pathway that regulates blood pressure and fluid balance in the body. Within this system, the hormone Angiotensin II acts as a powerful vasoconstrictor, meaning it causes blood vessels to narrow, which raises blood pressure.
Losartan’s mechanism of action involves selectively blocking the Angiotensin II Type 1 (AT1) receptors found on blood vessel walls and other tissues. By preventing Angiotensin II from binding to these specific receptors, Losartan stops the hormone from triggering its constricting effects. This blockade causes the blood vessels to relax and widen, a process called vasodilation, which ultimately lowers blood pressure.
The drug also reduces the release of aldosterone, a hormone that causes the body to retain sodium and water, further contributing to lower blood pressure and reduced fluid volume. Losartan is also indicated to reduce the risk of stroke in patients with high blood pressure and an enlarged heart muscle (left ventricular hypertrophy) and to slow the progression of kidney damage in patients with type 2 diabetes. Losartan’s active metabolite is more potent than the parent drug, supporting its once-daily dosing.
Understanding Angiotensin-Converting Enzyme Inhibitors
Angiotensin-Converting Enzyme (ACE) inhibitors, such as Lisinopril and Enalapril, represent the other major class of drugs used to target the RAAS. This class also works to reduce the effects of Angiotensin II, but they do so by inhibiting its production rather than blocking its final action. The ACE enzyme is responsible for converting the inactive peptide Angiotensin I into the active, blood-pressure-raising hormone Angiotensin II.
By blocking the ACE enzyme, these drugs reduce the overall amount of Angiotensin II circulating in the bloodstream. Less Angiotensin II means less potent vasoconstriction and a lower release of aldosterone, leading to lower blood pressure. ACE inhibitors share many therapeutic uses with ARBs, including the treatment of hypertension, heart failure, and slowing kidney disease progression, particularly in diabetic patients.
However, the difference in the specific molecular target within the RAAS pathway defines the two distinct drug classes. The ACE enzyme is present in many parts of the body, which explains why blocking it can have effects beyond just blood pressure regulation.
Key Differences in Mechanism and Clinical Profile
The primary distinction between ACE inhibitors and ARBs like Losartan lies in where they interrupt the RAAS pathway. ACE inhibitors act “upstream” by preventing the production of Angiotensin II, while ARBs act “downstream” by blocking the final binding site—the AT1 receptor—of Angiotensin II. This difference means that while ACE inhibitors reduce the overall supply of the hormone, ARBs ensure that any Angiotensin II that is still produced cannot exert its harmful effects on blood vessels.
A significant clinical difference arises from the fact that ACE inhibitors block the enzyme responsible for breaking down a substance called bradykinin. When ACE is inhibited, bradykinin levels increase, and this accumulation is widely believed to be the cause of the persistent, dry, irritating cough experienced by up to 10% of patients taking ACE inhibitors. Losartan and other ARBs do not affect the ACE enzyme or bradykinin levels, meaning they rarely cause this specific cough.
This difference in side effect profile is the main reason a physician may switch a patient from an ACE inhibitor to an ARB. Patients who cannot tolerate the cough associated with drugs like Lisinopril are often successfully treated with Losartan. Both drug classes carry a risk of a serious side effect called angioedema (swelling of the face, tongue, or throat), but the risk may be slightly lower for ARBs compared to ACE inhibitors.