Angiotensin II receptor blockers (ARBs); Types, Uses, Effects

Last updated: February 7, 2026Reviewed date: February 7, 2026Reading time: 8 min read
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Angiotensin II receptor blockers (ARBs), also known as angiotensin II receptor antagonists, AT1 receptor antagonists or sartans, are a group of pharmaceuticals that modulate the renin-angiotensin system. Their main uses are in the treatment of hypertension (high blood pressure), diabetic nephropathy(kidney damage due to diabetes) and congestive heart failure. They block the activation of AT1 receptors, preventing the binding of angiotensin II. or Angiotensin...

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Article Summary

Angiotensin II receptor blockers (ARBs), also known as angiotensin II receptor antagonists, AT1 receptor antagonists or sartans, are a group of pharmaceuticals that modulate the renin-angiotensin system. Their main uses are in the treatment of hypertension (high blood pressure), diabetic nephropathy(kidney damage due to diabetes) and congestive heart failure. They block the activation of AT1 receptors, preventing the binding of angiotensin II. or Angiotensin II is a hormone that may act on the central nervous system to regulate renal sympathetic nerve activity, renal function, and,...

Key Takeaways

  • This article explains Types of Angiotensin II receptor blockers in simple medical language.
  • This article explains Mechanism of action of Angiotensin II receptor blockers in simple medical language.
  • This article explains Indications  of Angiotensin II receptor blockers in simple medical language.
  • This article explains Contra-Indications of Angiotensin II receptor blockers in simple medical language.
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Definition

Angiotensin II receptor blockers (ARBs), also known as angiotensin II receptor antagonists, AT1 receptor antagonists or sartans, are a group of pharmaceuticals that modulate the renin-angiotensin system. Their main uses are in the treatment of hypertension (high blood pressure), diabetic nephropathy(kidney damage due to insulin is low or not working well. সহজ বাংলা: রক্তে চিনি বেশি থাকার রোগ।" data-rx-term="diabetes" data-rx-definition="Diabetes is a condition where blood sugar stays too high because insulin is low or not working well. সহজ বাংলা: রক্তে চিনি বেশি থাকার রোগ।">diabetes) and congestive heart failure. They block the activation of AT1 receptors, preventing the binding of angiotensin II.

or

Angiotensin II is a hormone that may act on the central nervous system to regulate renal sympathetic nerve activity, renal function, and, therefore, blood pressure. Angiotensin II is produced locally within the kidney and mediates tissue injury through a series of nonhemodynamic effects. angiotensin II is not only involved in the regulation of blood pressure, water, and sodium homeostasis, and control of other neurohumoral systems, but also leads to excessive production of reactive oxygen species and to hypertrophy, proliferation, migration, and apoptosis of vascular cells. Angiotensin II is one of the main factors involved in hypertension-induced tissue damage. This peptide regulates the inflammatory process. Angiotensin II activates circulating cells and participates in their adhesion to the activated endothelium and subsequent transmigration through the synthesis of adhesion molecules, chemokines, and cytokines. Among the intracellular signals involved in angiotensin II-induced infection, or irritation, often causing pain, swelling, heat, or redness. সহজ বাংলা: শরীরের প্রদাহ; ব্যথা, ফোলা বা লালভাব হতে পারে।" data-rx-term="inflammation" data-rx-definition="Inflammation is the body’s response to injury, infection, or irritation, often causing pain, swelling, heat, or redness. সহজ বাংলা: শরীরের প্রদাহ; ব্যথা, ফোলা বা লালভাব হতে পারে।">inflammation, the production of reactive oxygen species and the activation of nuclear factor-kappaB are the best known. Classical, well-defined actions of Angiotensin II in the brain include the regulation of hormone formation and release, the control of the central and peripheral sympathoadrenal systems, and the regulation of water and sodium intake. As a consequence of changes in the hormone, sympathetic and electrolyte systems, feedback mechanisms, in turn, modulate the activity of the brain Angiotensin II systems. There are two Angiotensin II systems in the brain. The discovery of brain Angiotensin II receptors located in neurons inside the blood-brain barrier confirmed the existence of an endogenous brain Angiotensin II system, responding to Angiotensin II generated in and/or transported into the brain. In addition, Angiotensin II receptors in circumventricular organs and in cerebrovascular endothelial cells respond to circulating Angiotensin II of peripheral origin. Thus, the brain responds to both circulating and tissue Angiotensin II, and the two systems are integrated. [1](PMID: 17147923, 16672146, 16601568, 16481883, 16075377).

Types of Angiotensin II receptor blockers

Pressor inhibition

Pressor inhibition at trough level – this relates to the degree of blockade or inhibition of the blood pressure-raising (“pressor”) effect of angiotensin II. However, pressor inhibition is not a measure of blood pressure-lowering (BP) efficacy per se. The rates as listed in the US FDA Package Inserts (PIs) for inhibition of this effect at the 24th hour for the ARBs are as follows: (all doses listed in PI are included)

  • Valsartan 80 mg 30%
  • Telmisartan 80 mg 40%
  • Losartan 100 mg 25–40%
  • Irbesartan 150 mg 40%
  • Irbesartan 300 mg 60%
  • Azilsartan 32 mg 60%
  • Olmesartan 20 mg 61%
  • Olmesartan 40 mg 74%

AT1 affinity

AT1 affinity vs AT2 is not a meaningful efficacy measurement of BP response. The specific AT1 affinity relates to how specifically attracted the medicine is for the correct receptor, the US FDA PI rates for AT1affinity are as follows:

  • Losartan 1000-fold
  • Telmisartan 3000-fold
  • Irbesartan 8500-fold
  • Candesartan greater than 10000-fold
  • Olmesartan 12500-fold
  • Valsartan 30000-fold
  • Saprisartan

Biological half-life

The third area needed to complete the overall efficacy picture of an ARB is its biological half-life. The half-lives from the US FDA PIs are as follows:

  • Valsartan 6 hours
  • Losartan 6–9 hours
  • Azilsartan 11 hours
  • Irbesartan 11–15 hours
  • Olmesartan 13 hours
  • Telmisartan 24 hours
  • Fimasartan 7–11 hours

Overall classification

Mechanism of action of Angiotensin II receptor blockers

These substances are AT1-receptor antagonists; that is, they block the activation of angiotensin II AT1 receptors. Blockage of AT1 receptors directly causes vasodilation, reduces secretion of vasopressin, and reduces production and secretion of aldosterone, among other actions. The combined effect reduces blood pressure.The specific efficacy of each ARB within this class depends upon a combination of three pharmacodynamic and pharmacokinetic parameters. Efficacy requires three key PD/PK areas at an effective level; the parameters of the three characteristics will need to be compiled into a table similar to one below, eliminating duplications and arriving at consensus values; the latter is at variance now.

or

As part of the renin-angiotensin-aldosterone-system (RAAS), angiotensin II raises blood pressure by vasoconstriction, increased aldosterone release by the adrenal zona glomerulosa, sodium and water reabsorption in the proximal tubular cells, and vasopressin secretion [FDA Label, A31494] The direct action of angiotensin II on surrounding vessel walls is facilitated by binding to the G-protein-coupled angiotensin II receptor type 1 (AT-1) on vascular smooth muscle cells, which stimulates Ca2+/calmodulin-dependent phosphorylation of myosin and causes smooth muscle contraction that results in vasoconstriction [FDA Label, A31494]. The RAAS is ultimately regulated by a negative feedback effect of angiotensin II on renin production by the juxtaglomerular cells of the renal afferent arteriole. Unresuscitated septic shock associated with marked hypovolemia, extracellular fluid volume depletion, decreased cardiac output, low arterial blood pressure and decreased systemic vascular resistance causes an increase in renin secretion by the juxtaglomerular cells, resulting in elevated angiotensin II plasma levels and an increased secretion of aldosterone from the adrenal cortex. Angiotensin II binding to AT-1 receptors causes dose-dependent vasoconstriction of both afferent and efferent glomerular arterioles. The most pronounced effect of angiotensin II results on efferent arterioles, resulting in reduced renal blood flow and increased glomerular filtration pressure. [2]

Indications  of Angiotensin II receptor blockers

Contra-Indications of Angiotensin II receptor blockers

  • Porphyria
  • An acute syndrome of the heart
  • Severe narrowing of the aortic heart valve
  • Severe heart failure
  • Abnormally low blood pressure
  • Kidney disease with a reduction in kidney function
  • Fluid Retention in the Legs, arms or hands
  • Blood circulation failure due to the serious heart condition
  • Chronic idiopathic constipation
  • Stomach or intestine blockage
  • Narrowing of the intestines
  • Decreased motility function of stomach or itestines
  • Heart attack
  • Allergies to calcium channel blockers
  • Calcium channel blocking agents-dihydropyridines
  • Symptomatic left ventricular ejection fraction ≤ 35% Chronic heart failure
  • Treatment of uncomplicated hypertension, isolated systolic hypertension and left ventricular hypertrophy.
  • Coronary artery disease in those intolerant of ACE inhibitors.
  • Pediatric hypertension 6 to 16 years of age.
  • Post-myocardial infarction.

Side Effects

The most common 

More common

Rare

Drug Interactions of Angiotensin II receptor blockers

Angiotensin II receptor blockers may interact with the following drug, supplements, & may change the efficacy of the drug

References

 

Angiotensin II receptor blockers (ARBs); Types, Uses, Effects

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Care roadmap for: Angiotensin II receptor blockers (ARBs); Types, Uses, Effects

Use this simple roadmap to understand the next safe steps. It is educational and does not replace examination by a doctor.

Go to emergency care if you notice:
  • Severe or rapidly worsening symptoms
  • Breathing difficulty, chest pain, fainting, confusion, severe weakness, major injury, or severe dehydration
Doctor / service to discuss: Qualified healthcare provider; specialist depends on symptoms and examination.
  1. Step 1

    Check danger signs first

    If danger signs are present, seek emergency care and do not wait for online information.

  2. Step 2

    Record the symptom story

    Write when symptoms started, severity, medicines already taken, allergies, pregnancy status, and test results.

  3. Step 3

    Visit a qualified clinician

    A doctor, nurse, or qualified healthcare provider can examine you and decide which tests or treatment are needed.

  4. Step 4

    Do only useful tests

    Do tests after clinical assessment. Avoid unnecessary tests, random antibiotics, or repeated medicines without diagnosis.

  5. Step 5

    Follow up and return early if worse

    If symptoms worsen, new warning signs appear, or treatment is not helping, return for review quickly.

Rural patient practical tips
  • Take a written symptom diary and all previous prescriptions/test reports.
  • Do not hide medicines already taken, even herbal or over-the-counter medicines.
  • Ask which warning signs mean urgent referral to hospital.

This roadmap is for education. A real diagnosis and treatment plan requires history, examination, and clinical judgment.

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Frequently Asked Questions

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