Olmesartan is classified as an Angiotensin II Receptor Blocker (ARB), not an Angiotensin-Converting Enzyme (ACE) Inhibitor. This medication belongs to a class of drugs used primarily to treat high blood pressure and heart failure. While both ARBs and ACE Inhibitors serve the same overarching purpose of lowering blood pressure, they achieve this result by intervening at different points within the body’s complex regulatory system.
Olmesartan’s Classification: The Role of ARBs
Olmesartan, often prescribed under the brand name Benicar, functions by directly blocking a specific protein receptor found on blood vessels and other organs. It works by occupying the Angiotensin II Type 1 (AT1) receptor site, which prevents the hormone Angiotensin II from binding to it.
Angiotensin II is a powerful chemical that causes muscles surrounding blood vessels to contract, leading to vasoconstriction. By blocking the AT1 receptor, Olmesartan prevents this signal from reaching the smooth muscle cells, allowing the blood vessels to relax and widen. This widening reduces the resistance to blood flow, which in turn lowers blood pressure.
Angiotensin II normally stimulates the release of aldosterone, a hormone that promotes the retention of sodium and water in the body. By blocking the AT1 receptor, ARBs suppress this aldosterone release, leading to a mild increase in sodium and water excretion. This reduction in fluid volume further contributes to the overall blood pressure-lowering effect.
How ACE Inhibitors Differ
ACE Inhibitors operate earlier in the body’s chemical cascade than ARBs, targeting the production of the hormone instead of its final action. These medications inhibit the Angiotensin-Converting Enzyme (ACE), which is responsible for transforming a precursor protein, Angiotensin I, into the active form, Angiotensin II. By blocking this specific enzyme, ACE Inhibitors reduce the total amount of Angiotensin II circulating in the bloodstream.
This reduction in Angiotensin II leads to the same desired outcome as ARBs: blood vessel relaxation and lowered blood pressure. However, ACE Inhibitors do not completely stop the production of Angiotensin II, as other enzymes in the body can also contribute to its formation.
The ACE enzyme also plays a role in breaking down a substance called bradykinin. When an ACE Inhibitor blocks the enzyme, it prevents the breakdown of bradykinin, leading to an accumulation of this substance in the body. This accumulation is responsible for certain side effects unique to the ACE Inhibitor class of drugs.
The Common Pathway: Regulating the Renin-Angiotensin System
Both Olmesartan (an ARB) and ACE Inhibitors regulate blood pressure by targeting components of the Renin-Angiotensin-Aldosterone System, often referred to as RAAS. The process begins when specialized cells in the kidneys release the enzyme renin, typically in response to low blood pressure or low fluid volume.
Renin acts on a substance from the liver called angiotensinogen to create Angiotensin I. Angiotensin I then travels through the bloodstream and is converted into the potent hormone Angiotensin II by the Angiotensin-Converting Enzyme (ACE). Angiotensin II is the main effector of the system, causing blood vessels to constrict and stimulating the adrenal glands to release aldosterone.
This is the point where the two drug classes intervene in distinct ways. ACE Inhibitors block the ACE enzyme, preventing the conversion step that creates Angiotensin II. Conversely, ARBs like Olmesartan allow Angiotensin II to be created, but they block the receptor that the hormone must bind to in order to exert its pressure-raising effects.
Practical Comparison: Choosing Between ARBs and ACE Inhibitors
The most notable difference between ARBs and ACE Inhibitors is the incidence of a specific side effect: a persistent, dry cough. This cough is reported in a significant percentage of patients taking an ACE Inhibitor.
The mechanism behind the cough is the buildup of bradykinin, which occurs because the ACE enzyme is blocked from breaking it down. Since ARBs do not affect the ACE enzyme, they do not cause this same accumulation of bradykinin. Consequently, patients who develop an intolerable cough while taking an ACE Inhibitor are often successfully transitioned to an ARB like Olmesartan.
Another rare but potentially serious difference is the risk of angioedema, which is swelling of the face, lips, tongue, or throat. While both drug types carry a risk of angioedema, the incidence is significantly lower with ARBs compared to ACE Inhibitors. This lower risk, combined with the decreased likelihood of cough, makes ARBs a preferred alternative for patients unable to tolerate the side effects associated with ACE Inhibitors.