Management of hypertension: the advent of a new angiotensin II receptor antagonist.
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type 1 (AT1) receptor antagonists have received increased therapeutic recognition in the treatment of hypertension. Although the overall effects of the ACE inhibitors and AT1 receptor antagonists may seem superficially similar, there are important differences between the two classes in terms of neurohumoral activation, concomitant bradykinin potentiation, and inhibition of angiotensin II, derived not only from the classical ACE pathway, but also from alternative pathways. The AT1 receptor antagonist eprosartan has been shown to lower blood pressure effectively in hypertensive patients. When taken in the recommended dose range, 600-800 mg once daily, eprosartan is effective in patients with all grades of hypertension, regardless of age, sex or race. In several clinical studies, the blood-pressure-lowering effect of eprosartan has been shown to be at least as great as that of the ACE inhibitor enalapril. With respect to tolerability, eprosartan is superior to ACE inhibitor therapy and comparable to placebo. The pharmacological and therapeutic profiles of the expanding array of AT1 receptor antagonists differ in a number of respects. Most of these agents are biphenyl tetrazole, non-competitive antagonists, and some have active metabolites. Eprosartan differs from other AT1 receptor antagonists in that it is a non-biphenyl, non-tetrazole competitive antagonist without active metabolites. Several large-scale, ongoing clinical research programmes (e.g. LIFE, SCOPE and VALUE) are expected to provide information on the extent to which AT1 receptor antagonists, in comparison with other therapeutic regimens, reduce cardiovascular morbidity and mortality in different groups of hypertensive subjects. Meanwhile, current evidence suggests that the AT1 receptor antagonists provide a new approach to the management of hypertension and that they merit a fuller assessment in other cardiovascular diseases.
Hedner
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Department of Clinical Pharmacology, Sahlgrenska University Hospital, Gothenburg, Sweden. thomas.hedner@pharm.gu.se
D000179:Acrylates / Q000627:therapeutic use*; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D004656:Enalapril / Q000627:therapeutic use*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000401:mortality / Q000503:physiopathology; D007093:Imidazoles / Q000627:therapeutic use*; D015996:Survival Rate; D013876:Thiophenes; D016896:Treatment Outcome
D000179:Acrylates; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D007093:Imidazoles; D013876:Thiophenes; C068373:eprosartan; D004656:Enalapril