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Eprosartan

A Review of its Use in the Management of Hypertension

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Summary

Abstract

Eprosartan is a potent and selective angiotensin II subtype 1 receptor antagonist. Results of large (n > 100) randomised double-blind studies in patients with mild, moderate or severe hypertension demonstrated that the antihypertensive efficacy of eprosartan (usually 400 to 800 mg/day as a single daily dose or in 2 divided doses) is significantly greater than that of placebo and at least as good as that of enalapril. In placebo-controlled trials, eprosartan achieved mean reductions from baseline in trough sitting systolic blood pressure of 6.3 to 15mm Hg and in diastolic blood pressure of 4.1 to 9.7mm Hg. Response rates associated with once daily administration of eprosartan 400 to 800mg were approximately double those with placebo.

Overall, eprosartan was well tolerated with a similar tolerability profile to that of placebo. In comparative trials, in which the incidence of persistent dry cough was evaluated as the primary end-point, enalapril was several-fold more likely to induce this adverse event than eprosartan (the difference being statistically significant regardless of study population and definition of cough).

In conclusion, the angiotensin II receptor antagonist eprosartan is a well tolerated and effective antihypertensive agent that is administered once or twice daily without regard to meals. Eprosartan has a low potential for serious adverse events, and the drug has not been associated with clinically significant drug interactions. Unlike ACE inhibitors such as enalapril, eprosartan does not have a high propensity to cause persistent nonproductive cough. Thus, eprosartan represents a useful therapeutic option in the management of patients with hypertension.

Pharmacodynamic Properties

Eprosartan is a potent and selective antagonist of the angiotensin II subtype 1 (AT1) receptor, which mediates the well known effects of angiotensin II, such as vasoconstriction, aldosterone release and renal sodium handling. In animal tissues, high concentrations of eprosartan had no affinity for any other receptor types [e.g. angiotensin II subtype 2 (AT2), adrenergic, serotonergic]. AT2 receptor antagonists such as eprosartan have no effect on the breakdown of peptides such as bradykinin, whereas ACE inhibitors are associated with bradykinin potentiation, an effect that may be implicated in the development of persistent nonproductive cough.

Functional antagonism of AT1 receptor-mediated activity was demonstrated in a variety of in vitro analyses, using animal tissues and cloned human AT1 receptors, and in several in vivo studies in animal models and in healthy volunteers and patients with hypertension. Overall, results of these studies demonstrated that eprosartan inhibited various physiological effects associated with angiotensin II (e.g. contractile responses in rabbit aortic rings, isotonic fluid absorption in rabbit perfused proximal convoluted tubules, pressor responses in animal models and healthy volunteers), and demonstrated true competitive antagonism in studies that investigated this characteristic. Increasing doses of other AT1 receptor antagonists produced a rightward shift of the angiotensin concentration-response curve but, unlike eprosartan, also reduced the maximum responses to angiotensin II. In a rat model of severe hypertension, eprosartan markedly reduced mortality and ECG evidence of cardiac hypertrophy.

Eprosartan had equal affinity for postsynaptic (vascular) and presynaptic (neuronal) AT1 receptors in in vitro studies, whereas losartan inhibited only postsynaptic AT1 receptors. In in vivo studies involving single dose parenteral administration of eprosartan and other AT1 receptor antagonists to small numbers of pithed rats, only eprosartan inhibited presynaptic (as well as postsynaptic) sympathetic outflow. However, whether these findings translate into a potential clinical advantage of eprosartan over other agents has yet to be demonstrated.

In healthy volunteers with an activated renin-angiotensin system or in those receiving exogenous angiotensin II, eprosartan reduced blood pressure and plasma aldosterone levels, and increased urinary sodium excretion, renal plasma flow and plasma renin activity. In patients with hypertension or renal insufficiency, eprosartan had no effect on glomerular filtration rate, renal plasma flow or sodium excretion. Eprosartan (unlike losartan) does not appear to have uricos-uric activity.

Pharmacokinetic Properties

The pharmacokinetic properties of eprosartan after oral administration have been determined primarily in healthy adults, although limited data in patients with hypertension appear to be similar. Oral bioavailability is approximately 13% and is not significantly affected by food. Time to achieve maximum plasma drug concentration ranges from 1 to 3 hours depending on food intake (i.e. food tends to delay eprosartan absorption). Eprosartan has a volume of distribution of approximately 13L and is highly bound to plasma proteins (∼98%). Approximately two-thirds of eprosartan reaching the systemic circulation is eliminated unchanged by biliary excretion, the remaining one-third is eliminated in the urine primarily as unchanged drug. Approximately 20% of renal elimination of eprosartan is as the acyl glucuronide. The drug has an elimination half-life of approximately 4.5 to 9 hours.

No differences were noted in the pharmacokinetic properties of eprosartan between healthy men and women, but area under the concentration-time curve (AUC0–∞) and peak plasma concentration (Cmax) were about twice as high in elderly versus younger volunteers. AUC values were also increased by about 40 to 50% in patients with chronic liver disease and by approximately 25 to 55% in patients with moderate to severe renal impairment compared with healthy volunteers. However, in view of the good tolerability profile of the drug, none of these differences were deemed significant enough to warrant initial dosage adjustments of eprosartan.

Eprosartan is not metabolised by the cytochrome P450 (CYP) enzyme system and in vitro studies indicate that the drug does not inhibit a variety of CYP isoenzymes (e.g. CYP2C9, CYP3A); therefore, the drug has a low potential for pharmacokinetic drug interactions. Indeed, several studies (typically in healthy volunteers but sometimes in patients with specific disorders such as type 2 diabetes mellitus) have been undertaken evaluating the effect of eprosartan on plasma concentrations or pharmacodynamic effects of other drugs [e.g. digoxin, warfarin, glibenclamide (glyburide)]. Eprosartan was found to have no clinically significant interactions. Studies of concomitant administration of known CYP inhibitors (e.g. fluconazole, ketoconazole) also showed no effect of these drugs on the pharmacokinetics of eprosartan.

Therapeutic Efficacy

Results of randomised, double-blind, placebo-controlled, multicentre trials in >100 patients consistently demonstrated statistically significant differences in antihypertensive efficacy favouring eprosartan 400 to 800 mg/day (as a single daily dose or in 2 divided doses) over placebo. Eprosartan achieved mean reductions from baseline in trough sitting diastolic blood pressure (DBP; primary efficacy end-point) ranging from 4.1 to 9.7mm Hg and corresponding reductions in systolic blood pressure (SBP) of 6.3 to 15mm Hg. Mean reductions in sitting DBP with placebo were 0.1 to 4mm Hg and mean changes in sitting SBP ranged from a small increase of 0.9mm Hg to a reduction of 4mm Hg. Response rates (percentage of patients with sitting DBP <90mm Hg or ≥10mm Hg reduction from baseline) were approximately twice as high with once daily administration of eprosartan than placebo (42 and 47% with eprosartan vs 21 or 26% with placebo; p < 0.05 for both comparisons) in 2 studies evaluating this parameter.

In 3 randomised comparisons with enalapril, the main efficacy results showed that eprosartan is at least as effective as enalapril, whether used as monotherapy or in combination with hydrochlorothiazide. In the largest study (n = 528) eprosartan (200 or 300mg twice daily) and enalapril (5 to 20mg once daily) were similarly effective at reducing sitting SBP/DBP after 26 weeks of therapy (15.5/12.9 vs 14.7/11.9mm Hg), but the antihypertensive response rate was significantly greater with eprosartan at both 12 (70 vs 63%; p < 0.05) and 26 (82 vs 73%; p < 0.05) weeks. Approximately 30% of patients in both treatment groups required concomitant hydrochlorothiazide therapy. It is noteworthy, however, that in this and 1 of the other comparative trials, the primary end-point was the incidence of persistent cough. Likewise, antihypertensive efficacy parameters were secondary end-points in a smaller 4-week comparison between eprosartan and losartan (n = 60), in which blood pressure reductions and response rate tended to favour eprosartan (not statistically significant).

Various subgroup analyses of larger studies comparing eprosartan with placebo or enalapril showed good antihypertensive activity with eprosartan regardless of age or gender. Eprosartan also provided a more consistent antihypertensive effect than enalapril in African-American patients on the basis of a small retrospective subgroup analysis.

Tolerability

Adverse events were reported by a similar proportion of patients with hypertension receiving eprosartan or placebo (54.4 vs 52.8%) and the rate of discontinuation of therapy because of adverse events was also similar (4 vs 6.5%) according to pooled data from placebo-controlled clinical trials (n = 1554). The most frequently reported adverse events with both eprosartan and placebo in these studies were headache (10.1 vs 10.8%), upper respiratory tract infection (7.9 vs 5.4%), myalgia (4.0 vs 4.0%), rhinitis (4.0 vs 2.9%), pharyngitis (3.7 vs 2.6%) and cough (3.5 vs 2.6%).

Comparative trials with enalapril showed that both drugs were similarly well tolerated. However, the incidence of persistent, dry, unproductive cough was several-fold higher (varied widely depending on the study population and definition of cough) among enalapril recipients in 2 studies for which this parameter was the primary end-point. The differences between treatment groups was statistically significant for both strict and less rigid definitions of persistent cough. One of the trials showed a 90% relative reduction in ‘definite’ cough when eprosartan was compared with enalapril in 111 patients with a history of enalapril-induced cough (2.6 vs 25.0%; p < 0.01).

Dosage and Administration

The usual recommended starting dosage of eprosartan is 600mg once daily in patients with hypertension receiving the drug as monotherapy. The recommended dosage range is 400 to 800 mg/day administered as a single daily dose or as 2 divided doses. If necessary, the drug may be used in combination with other antihypertensive drugs (e.g. thiazide diuretics or calcium antagonists).

In general, initial dosage adjustments of eprosartan are not necessary in patients with renal or hepatic impairment or in elderly patients. Patients who are volume-and/or salt-depleted (e.g. from diuretics) may develop symptomatic hypotension, and these conditions should be corrected prior to administration of eprosartan.

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Correspondence to Greg L. Plosker.

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Various sections of the manuscript reviewed by: I. Gavras, Hypertension and Atherosclerosis Section, Boston University School of Medicine, Boston, Massachusetts, USA; A.H. Gradman, Division of Cardiovascular Diseases, Western Pennsylvania Hospital, Pittsburgh, Pennsylvania, USA; G.D. Johnston, Department of Therapeutics and Pharmacology, Queen’s University of Belfast, Belfast, Northern Ireland; B. Levine, Department of Medicine, VA Medical Center, Los Angeles, California, USA; B.N.C. Prichard, Centre for Clinical Pharmacology, University College, London, England; M. Ravid, Department of Medicine, Meir Hospital, Kfar-Sava, Israel; D.A. Sica, Department of Clinical Pharmacology and Hypertension, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA.

Data Selection

Sources: Medical literature published in any language since 1983 on eprosartan, identified using AdisBase (a proprietary database of Adis International, Auckland, New Zealand), Medline and EMBASE. Additional references were identified from the reference lists of published articles. Bibliographical information, including contributory unpublished data, was also requested from the company developing the drug.

Search strategy: AdisBase search terms were ‘Eprosartan’ or ‘SKF-108566’. Medline search terms were ‘Eprosartan’ or ‘SKF-108566’. EMBASE search terms were ‘Eprosartan’ or ‘SKF-108566’. Searches were last updated 20 June 2000.

Selection: Studies in patients with hypertension who received eprosartan. Inclusion of studies was based mainly on the methods section of the trials. When available, large, well controlled trials with appropriate statistical methodology were preferred. Relevant pharmacodynamic and pharmacokinetic data are also included.

Index terms: Eprosartan, hypertension, antihypertensive, pharmacodynamics, pharmacokinetics, therapeutic use, drug interactions, tolerability.

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Plosker, G.L., Foster, R.H. Eprosartan. Drugs 60, 177–201 (2000). https://doi.org/10.2165/00003495-200060010-00009

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