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Angiotensin II receptor antagonists/blockers (ARBs) antagonize angiotensin II at the AT1 receptors in tissues, such as smooth muscle and the adrenal gland. Angiotensin II, a potent vasoconstrictor, is the primary vasoactive hormone of the renin-angiotensin-aldosterone system (RAAS) and plays an important role in the pathophysiology of hypertension and congestive heart failure. Two angiotensin II type receptors, AT1 and AT2, have been identified. Stimulation of the AT1 receptor by angiotensin II results in proliferation of smooth and cardiac muscle cells; promotion of cell growth; reabsorption of sodium from the renal proximal tubules; retention of water; vasoconstriction; stimulation of the synthesis and secretion of aldosterone and activation of the sympathetic system. Stimulation of the AT2 receptor results in vasodilation, production of nitric oxide and bradykinin and antiproliferative effects. Through selective antagonism of the AT1 receptors in tissues, such as vascular smooth muscle and the adrenal gland, the ARBs block vasoconstrictor and aldosterone-secreting effects of angiotensin II without a marked change in heart rate. Circulating levels of renin and angiotensin II rise in response to blockade of the AT1 receptors and, subsequently, increased stimulation of the AT2 receptor by angiotensin II. ARBs do not inhibit the angiotensin converting enzyme (ACE) and, thus, do not inhibit the breakdown of bradykinin.
Apart from the blood pressure reduction properties of the ARBs, there is evidence to suggest that molecular effects play a role in their clinical effectiveness. The identification and role of these molecular effects, as well as, whether they are medication specific or a class effect require further research. The clinical significance of the differences in the degree of binding affinity, selectivity, and insurmountability for the AT1 receptor between ARBs remains unknown.
Dose Range and Equivalence for ARBs in Hypertension
40 to 80 mg
25 to 50 mg
80 to 160 mg
Dose Range (mg/day)
8 to 32 mg
150 to 300 mg
50 to 100 mg
20 to 40 mg
20 to 80 mg
80 to 320 mg
Once or Twice Daily
Greater Affinity for AT1 Receptor than AT2
*The approximate equivalence is based on data from clinical trials and meta-analyses comparing 2 or more ARBs for hypertension; this approximation may not represent the equivalence for other indications.
Angiotensin Receptor Blocker Comparative Efficacy Trials
Randomized, multicenter, 8 week, double-blind trial in essential hypertension.
Olmesartan 20 mg one daily (n=145)
Losartan 50 mg once daily (n=146)
Valsartan 80 mg once daily (n=142)
Irbesartan 150 mg once daily (n=145)
Results versus olmesartan
8 Week Mean Reduction in Cuff BP
Olmesartan: 11.5 mmHg
Losartan: 8.2 mmHg (p=0.0002)
Valsartan: 7.9 mmHg (p<0.0001)
Irbesartan: 9.9 mmHg (p=0.0412)
Olmesartan: 11.3 mmHg
Losartan: 9.5 mmHg
Valsartan: 8.4 mmHg
Irbesartan: 11 mmHg
8 Week Mean Reduction 24-Hour ABPM
Olmesartan: 8.5 mmHg
Losartan: 6.2 mmHg (p<0.05)
Valsartan: 5.6 mmHg (p<0.05)
Irbesartan: 7.4 mmHg (p=0.087)
Olmesartan: 12.5 mmHg
Losartan: 9 mmHg (p<0.05)
Valsartan: 8.1 mmHg (p<0.05)
Irbesartan: 11.3 mmHg
Trough-to-Peak Ratios (DBP; SBP)
Olmesartan: 0.68; 0.69
Losartan: 0.69; 0.64
Valsartan: 0.48; 0.55
Irbesartan: 0.60; 0.62
The ARBs all reduced DBP and SBP; however, olmesartan associated with significantly greater reductions in cuff DBP (vs losartan, valsartan and irbesartan), ABPM DBP (vs losartan and valsartan; not irbesartan) and ABPM SBP (vs losartan and valsartan; not irbesartan).
There were no differences in safety profiles between therapies.
Randomized, multicenter, 6 week, double-blind, forced-titration trial in stage 1 and 2 hypertension.
Azilsartan 40 mg one daily (n=280)
Azilsartan 80 mg once daily (n=285)
Olmesartan 40 mg once daily (n=290)
Valsartan 320 mg once daily (n=282)
6 Week Mean Reduction 24-Hour ABPM
Placebo: 0.1 mmHg
Azilsartan: 40 mg: 8.7 mmHg
Azilsartan: 80 mg: 9.4 mmHg (p=0.011 vs olmesartan and p<0.001 vs valsartan)
Olmesartan: 7.1 mmHg
Valsartan: 7.7 mmHg
Placebo: 0.3 mmHg
Azilsartan: 40 mg: 13.4 mmHg
Azilsartan: 80 mg: 14.5 mmHg (p=0.009 vs olmesartan and p<0.001 vs valsartan)
Olmesartan: 12 mmHg
Valsartan: 10 mmHg
6 Week Mean Reduction Clinic BP
Placebo: 0.8 mmHg
Azilsartan: 40 mg: 7 mmHg (p=0.017 vs valsartan)
Azilsartan: 80 mg: 8.3 mmHg (p=0.005 vs olmesartan and p<0.001 vs valsartan)
Olmesartan: 6.1 mmHg
Valsartan: 5.1 mmHg
Placebo: 1.8 mmHg
Azilsartan: 40 mg: 16.4 mmHg (p=0.018 vs olmesartan and p<0.001 vs valsartan)
Azilsartan: 80 mg: 16.7 mmHg (p=0.008 vs olmesartan and p<0.001 vs valsartan)
Valsartan: 13.2 mmHg
Percentage of Patients with Clinic SBP < 140 mmHg and/or decrease of >/= 20 mmHg at 6 weeks
Azilsartan: 80 mg: 58% (p=0.05 vs olmesartan and valsartan)
Azilsartan 80 mg was found to provide statistically superior reductions in both DBP and SBP.
Further evaluation is needed to compare azilsartan to other ARBs.
Meta-analysis to compare valsartan efficacy in hypertension with 5 ARBs.
Candesartan 8 mg - 32 mg/day: 6 trials
Irbesartan 150 mg - 300 mg/day: 6 trials
Losartan 50 mg - 100 mg/day: 13 trials
Olmesartan 10 mg - 40 mg/day: 2 trials
Telmisartan 40 mg - 80 mg/day: 5 trials
Valsartan 80 mg - 320 mg/day: 12 trials
As compared to valsartan, mean change in SBP and DBP by drug and dose (only significant differences listed below)
SBP Reduction Greater with Valsartan
Irbesartan 150 mg vs Valsartan 160 mg: 3.56 mm Hg (95% CI: 0.77, 6.38)
Losartan 100 mg vs Valsartan 160 mg:
3.31 mmHg (95% CI: 0.86, 5.79)
Losartan 100 mg vs Valsartan 320 mg:
3.84 mmHg (95% CI: 1.34, 6.31)
DBP Reduction Greater with Valsartan
Candesartan 16 mg vs Valsartan 160 mg:
1.85 mmHg (95% CI: 0.34, 3.40)
Irbesartan 150 mg vs Valsartan 160 mg: 2.06 mm Hg (95% CI: 0.71, 3.45)
1.95 mmHg (95% CI: 0.81, 3.11)
2.6 mmHg (95% CI: 1.45, 3.76)
Valsartan 160 mg and 320 mg per day were more effective in SBP and DBP reduction compared to losartan 100 mg and valsartan 160 mg/day found to be more effective than irbesartan 150 mg/day.
Valsartan provides BP reductions comparable to other ARBs.
Meta-analysis to compare the eprosartan efficacy to other antihypertensive agents in the treatment of essential hypertension; included studies compared eprosartan to
Placebo: 8 trials
Losartan: 4 trials
Telmisartan: 2 trials
Valsartan: 1 trial
Enalapril: 8 trials
Nitrendipine: 1 trial
Atenolol: 1 trial
As compared to eprosartan, the weighted mean differences in SBP and DBP
Retrospective population-based study to compare the effectiveness of ARBs on morality in elderly patients with heart failure.
Adjusted Hazard Ratios (HR) with Losartan as the reference
Valsartan: 0.63 (95% CI: 0.51, 0.79)
Irbesartan: 0.65 (95% CI: 0.53, 0.79)
Candesartan: 0.71 (95% CI: 0.57, 0.90)
Telmisartan: 0.92 (95% CI: 0.55, 1.54)
Abbreviations: BP = blood pressure; DBP = diastolic blood pressure; SBP = systolic blood pressure; ABPM = ambulatory blood pressure monitoring
Cough, a well-described adverse effect of angiotensin-converting enzyme (ACE) inhibitors, has been reported at a lower incidence with angiotensin receptor blocker (ARB) therapy. ARBs do not inhibit the angiotensin converting enzyme (kinase II) or have an effect on other enzymes involved in the metabolism of substance P, or other peptides, which are thought to play a role in the development of ACE inhibitor-induced cough. ARBs may be an alternative for patients intolerant to ACE inhibitors due to cough.
There have been reports of angioedema (swelling of lips and eyelids, facial rash) and anaphylactic reactions with ARBs; theoretically the risk of angioedema should be less with ARBs compared to ACE inhibitors. Patients with a history of angioedema with an ACE inhibitor may be started on an ARB 6 weeks after discontinuation of the ACE inhibitor.
Evidence from animal studies and a meta-analysis suggest a potential association between ARBs and cancer; multiple other meta-analyses did not find an association.  In June 2011, the FDA announced completion of its review of the data and that the use of ARBs for hypertension does not increase the risk of cancer. Based on review of the literature, there does not appear to be a link between ARB therapy and development of cancer.
Elevations in serum creatinine and blood urea nitrogen can occur with ARB therapy; patients with renal impairment or bilateral renal artery stenosis are more likely to experience elevations. Oliguria, progressive azotemia, and, rarely, acute renal failure and/or death have been reported. Acute renal failure has occurred with ARB therapy in patients with bilateral renal artery stenosis. Renal function should be closely monitored during initial therapy.
Sprue-like enteropathy has been reported in patients taking olmesartan. The enteropathy developed months to years after initiating therapy. Symptoms include severe, chronic diarrhea with substantial weight loss (median 18 kg; range, 2.5 to 57 kg). Villous atrophy was often observed on intestinal biopsy. There have been rare reports of enteropathy with other ARBs suggesting a class effect.
Symptomatic hypotension has been reported with ARB therapy. If excessive hypotension occurs, the patient should be placed in the supine position and, if necessary, receive an intravenous infusion of normal saline. A transient hypotensive response is not a contraindication to further treatment with an ARB, which usually can be given without difficulty once the blood pressure has stabilized. If symptomatic hypotension develops, a dose reduction or discontinuation of the ARB or concomitant diuretic may be necessary.
Aliskiren-containing products are contraindicated in combination with an ARB in patients with diabetes mellitus and not recommended in patients with renal impairment (CrCl less than 60 mL/min). Do not coadminister two renin-angiotensin-aldosterone (RAAS) inhibitors, such as ACE inhibitors, ARBs or aliskiren. Combination therapy increases the risk for hyperkalemia, renal impairment, hypotension, and other side effects. Most patients receiving combination therapy with 2 RAAS inhibitors do not obtain any additional benefit compared to monotherapy.
Since ACE inhibitors have been associated with minor increases in serum potassium, clinically relevant hyperkalemia may occur during coadministration with agents that increase potassium. Some examples of medications that increase potassium include cyclosporine, eplerenone, drospirenone; ethinyl estradiol, potassium-sparing diuretics, potassium substitutes, potassium salts or salt substitutes, and trimethoprim. Monitor serum potassium levels during concomitant therapy.
Losartan is a substrate of CYP3A4 and CYP2C9; thus, coadministration with inhibitors or inducers of these isoenzymes may alter the systemic exposure to losartan. Valsartan is a substrate of the hepatic uptake transporter OATP1B1 and the hepatic efflux transporter MRP2. Coadministration of valsartan with OATP1B1 inhibitors (i.e., atazanavir, cyclosporine, daclatasvir, rifampin) or MRP2 inhibitors (i.e., ritonavir) may increase systemic exposure to valsartan. Telmisartan may have some inhibitory effects on CYP2C19 and may theoretically alter the metabolism of substrates of this isoenzyme.
Further deterioration of renal function, including acute renal failure, may occur in elderly, volume-depleted (including those on diuretic therapy), or renally impaired patients on both an ARB and nonsteroidal antiinflammatory drug (NSAID) or selective cyclooxygenase-2 inhibitors (COX-2 inhibitors); the effects are usually reversible. Monitor renal function in patients receiving concomitant therapy. Additionally, NSAIDs may reduce the antihypertensive effect of ARBs.
ARBs increase sodium excretion, which may result in increased reabsorption of lithium when the two agents are administered concomitantly. Monitor lithium levels, look signs of toxicity and adjust lithium dosage as needed when given with an ARB.
When pregnancy is detected, discontinue ARB therapy as soon as possible. Use of medications that affect the renin-angiotensin system, such as ARBs, during the second or third trimesters reduce fetal renal function, increase fetal and neonatal death, and cause fetal and neonatal injury such as hypotension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure, and death. Anhydramnios and oligohydraminos have also been reported. Women of childbearing age should be made aware of these harmful effects and consideration given to using another drug class.
Despite a low incidence of hyperkalemia with ARBs, there is a potential for these drugs to worsen existing hyperkalemia through inhibition of aldosterone secretion. Patients with heart failure, advanced renal impairment or those taking potassium-sparing diuretics, potassium supplements or salt substitutes may be at risk of developing hyperkalemia with ARB therapy.
Hypotension is an infrequent adverse effect of ARBs in patients with uncomplicated hypertension; however, it has been reported more frequently in patients with an activated renin-angiotensin-aldosterone system (e.g. heart failure, volume or salt depleted, high dose diuretics) and post-myocardial infarction. Volume and salt depletion should be corrected prior to initiation of ARB therapy. Lower initial doses of ARBs may be recommended. If hypotension occurs, standard medical care should be provided.
Hepatic impairment may alter the clearance of ARBs. Dose adjustments are recommended for candesartan, losartan, telmisartan in patients with moderate hepatic impairment. There is a lack of available data on the use of azilsartan, candesartan, losartan, and valsartan in patients with severe hepatic impairment. No dosage adjustments needed for irbesartan in patients with hepatic impairment.
Patients dependent on the RAAS for renal function, such as those with heart failure, may experience a worsening of renal function with ARB therapy. Unilateral or bilateral renal artery stenosis and elevated serum creatinine or blood urea nitrogen have been reported. Typically increases in serum creatinine, blood urea nitrogen and potassium are transient in heart failure patients on ARB therapy; however, oliguria, progressive azotemia and, rarely acute renal failure has occurred. Renal function should be monitored during ARB therapy.
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