Sartans, formally called Angiotensin II Receptor Blockers (ARBs), are a class of prescription medicines used to manage cardiovascular health. They are distinguished by the common suffix “-sartan” in their generic names, such as losartan and valsartan. ARBs are widely prescribed globally to treat conditions related to high blood pressure and heart function. They relax blood vessels, allowing blood to flow more easily throughout the body.
How Sartans Function in the Body
Sartans interfere with the Renin-Angiotensin System (RAS), the body’s primary mechanism for regulating blood pressure and fluid balance. The RAS pathway produces Angiotensin II, a powerful hormone and potent vasoconstrictor. When present, Angiotensin II signals blood vessel muscles to contract, causing the vessels to narrow and increasing blood pressure.
Sartans block the effects of Angiotensin II by selectively binding to and inhibiting the Angiotensin II type 1 (AT1) receptor. This receptor is responsible for the hormone’s constricting and pressure-raising effects. By occupying the AT1 receptor, the medication prevents Angiotensin II from attaching and signaling the vessel walls.
This targeted blockade leads to vasodilation, the relaxation and widening of arteries and veins. The resulting expansion of blood vessels reduces resistance to blood flow, effectively lowering systemic blood pressure. Blocking the AT1 receptor also indirectly reduces the secretion of aldosterone. Aldosterone causes the body to retain sodium and water, so its reduction decreases overall blood volume and reduces strain on the heart.
Medical Conditions They Treat
The primary use for sartans is the long-term management of high blood pressure (hypertension), a major risk factor for heart disease and stroke. By promoting vasodilation, these medications reduce the force exerted on artery walls, bringing blood pressure down. Regular use helps protect the vasculature from chronic damage associated with sustained high pressure.
Sartans are also a common treatment for heart failure, a condition where the heart muscle cannot pump blood effectively. The medications reduce the afterload (the resistance the heart must pump against), allowing the heart to work more efficiently. This reduction in strain helps limit the progressive remodeling and weakening of the heart muscle.
Sartans also protect the kidneys, particularly in patients with type 2 diabetes and high blood pressure. By lowering pressure within the kidney’s filtering units, sartans can slow the progression of diabetic nephropathy (kidney damage caused by diabetes). This renoprotective effect is a factor in their use for patients with co-existing cardiovascular and metabolic conditions.
Understanding Potential Side Effects
Sartans are generally well-tolerated, but users may experience common, mild side effects as the body adjusts. These frequently include dizziness or lightheadedness, often due to the blood pressure-lowering effect, especially when standing up quickly. Some individuals may also report fatigue or headache during the initial phase of treatment.
A more serious, though less frequent, concern is hyperkalemia (an elevated level of potassium in the blood). Because sartans interfere with the RAS, they can affect the body’s ability to excrete potassium, necessitating regular blood tests. High potassium levels can disrupt the heart’s electrical rhythm.
Sartans are contraindicated throughout all trimesters of pregnancy. Exposure to these medications, particularly during the second and third trimesters, has been linked to severe fetal and neonatal toxicity, including developmental issues. Risks involve potential kidney failure in the fetus and a reduction in amniotic fluid. Women who are pregnant or planning to become pregnant must consult their doctor immediately to switch to a safer alternative therapy.
How Sartans Compare to Other Medications
Sartans are often compared with Angiotensin-Converting Enzyme (ACE) inhibitors, as both target the same overarching system of blood pressure regulation. While ACE inhibitors block the enzyme that produces Angiotensin II, sartans work downstream by blocking the specific AT1 receptor that Angiotensin II binds to. Both drug classes achieve the goal of reducing the hormone’s pressor effects through different mechanisms.
The primary advantage of sartans is their more favorable side-effect profile compared to ACE inhibitors. ACE inhibitors often cause a persistent, dry cough because they inhibit the breakdown of bradykinin. Sartans do not affect the bradykinin pathway, which significantly reduces the incidence of this cough.
Sartans also carry a lower risk of angioedema, a rapid swelling of the deep layers of the skin, often affecting the face, tongue, and throat. For patients who develop a cough or angioedema while taking an ACE inhibitor, a sartan is typically the preferred alternative. This difference in side effects makes sartans a valuable second-line option for individuals who cannot tolerate first-line ACE inhibitor therapy.