Olmesartan
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sheng Shi, M.D. [2]
For patient information about Olmesartan, click here.
Synonyms / Brand Names: BENICAR®
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Overview
Olmesartan (Benicar®,Olmetec®) belongs to the class of medicines called angiotensin II receptor antagonists to treat high blood pressure. It is marketed worldwide by Daiichi Sankyo, Ltd. and in the United States by Daiichi Sankyo, Inc. and Forest Laboratories. Olmesartan works by blocking the binding of angiotension II to the AT1 receptors in vascular muscle; it is therefore independent of angiotension II synthesis pathways, unlike ACE inhibitors. By blocking binding rather than synthesis of angiotension II, olmesartan inhibits the negative regulatory feedback on renin secretion. As a result of this blockage, olmesartan restricts vasoconstriction and the secretion ofaldosterone. This lowers blood pressure by producing vasodilation, and decreasing peripheral resistance.
Category
Category:Angiotensin II receptor antagonists;Imidazoles;Tetrazoles;Carboxylate esters;Alcohols;Biphenyls;Cardiovascular Drugs
FDA Package Insert
Indications and Usage | Dosage and Administration | Dosage Forms and Strengths | Contraindications | Warnings and Precautions | Adverse Reactions | Drug Interactions | Use in Specific Populations | Overdosage | Description | Clinical Pharmacology | Nonclinical Toxicology | Clinical Studies | How Supplied/Storage and Handling | Patient Counseling Information | Labels and Packages
Mechanism of Action
AngiotensinII is formed from AngiotensinI in a reaction catalyzed by Angiotensinconverting enzyme (ACE, kininase II). AngiotensinII is the principal pressor agent of the renin-Angiotensinsystem, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation and renal reabsorption of sodium. Olmesartan blocks the vasoconstrictor effects of AngiotensinII by selectively blocking the binding of AngiotensinII to the AT1 receptor in vascular smooth muscle. Its action is, therefore, independent of the pathways forAngiotensinII synthesis.
An AT2 receptor is found also in many tissues, but this receptor is not known to be associated with cardiovascular homeostasis. Olmesartan has more than a 12,500-fold greater affinity for the AT1 receptor than for the AT2 receptor.
Blockade of the renin-Angiotensinsystem with ACE inhibitors, which inhibit the biosynthesis of AngiotensinII from AngiotensinI, is a mechanism of many drugs used to treat hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Because olmesartan medoxomil does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known.
Blockade of the AngiotensinII receptor inhibits the negative regulatory feedback of AngiotensinII on renin secretion, but the resulting increased plasma renin activity and circulating AngiotensinII levels do not overcome the effect of olmesartan on blood pressure.