title: Clinical profile of eprosartan.
abstract: Angiotensin II (AII) receptor blockers offer an alternative means of blocking the renin-angiotensin-aldosterone system (RAAS) to angiotensin converting enzyme (ACE) inhibitors. Being highly selective for the AII receptor subtype AT(1), AII receptor blockers may avoid side-effects associated with ACE inhibitor treatment, such as cough. Eprosartan is a non-biphenyl, non-tetrazole competitive blocker that is chemically distinct from other AII receptor blockers, which may account for differences in its pharmacological properties. It induces dual blockade of AT(1) receptors both presynaptically and postsynaptically, reducing sympathetic nerve activity to a significantly greater degree than other AT(1) receptor blockers. At the recommended dose of 600 mg once daily, eprosartan effectively lowers blood pressure (BP) in hypertensive patients to a similar degree as seen with other AII receptor blockers and ACE inhibitors. However, a greater proportion of patients achieved adequate BP control compared with enalapril. When eprosartan is given in combination with hydrochlorothiazide (HCTZ), it provides a significantly greater BP reduction compared with eprosartan alone. Eprosartan has a side-effect profile that is similar to placebo and to other AII receptor blockers, but is better than that of enalapril because it lacks the propensity to cause dry cough. Eprosartan is not metabolized by the cytochrome P450 enzyme system, and so has no interaction with drugs that affect this system. Eprosartan completely reverses renal vasoconstriction induced by AII and may, therefore, have further applications in situations where stimulation of the RAAS is a problem. In summary, eprosartan, alone or in combination with HCTZ, provides an effective and well-tolerated approach to lowering BP in patients with all grades of hypertension. Further development of eprosartan may offer therapeutic opportunities that go far beyond the current recommendations.
authors.affiliation: Vascular Risk Unit, Division of Internal Medicine, Hospital La Paz, Universidad Autónoma, Madrid, Spain. jgarciapuig@navegalia.com
authors.forename: Juan García
authors.initials: JG
authors.lastname: Puig
authors.forename: María A Martínez
authors.initials: MA
authors.lastname: López
authors.forename: Teresa Sancho
authors.initials: TS
authors.lastname: Bueso
authors.forename: José I
authors.initials: JI
authors.lastname: Bernardino
authors.forename: Rosa Torres
authors.initials: RT
authors.lastname: Jiménez
mesh_terms: D000179:Acrylates / Q000494:pharmacology* / Q000627:therapeutic use*; D000804:Angiotensin II / Q000187:drug effects / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology* / Q000627:therapeutic use*; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D013876:Thiophenes; D016896:Treatment Outcome
chemical_list: D000179:Acrylates; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D007093:Imidazoles; D013876:Thiophenes; D000804:Angiotensin II; C068373:eprosartan