Olmesartan detailed information: Difference between revisions
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{{Olmesartan}} | |||
{{CMG}}; {{AE}} {{SS}} | |||
'''''For patient information about Olmesartan, click [[Olmesartan (patient information)|here]].''''' | |||
{{SB}} BENICAR<sup>®</sup> | |||
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==Overview== | ==Overview== | ||
==Administration== | '''Olmesartan''' (Benicar®,Olmetec®) belongs to the class of medicines called [[angiotensin II receptor antagonist]]s to treat [[hypertension|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 [[Angiotensin|angiotension II]] to the AT<sub>1</sub> receptors in vascular muscle; it is therefore independent of angiotension II synthesis pathways, unlike [[ACE inhibitor]]s. 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 of[[aldosterone]]. 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== | |||
''' [[Olmesartan indications and usage|Indications and Usage]]''' | |||
'''| [[Olmesartan dosage and administration|Dosage and Administration]]''' | |||
'''| [[Olmesartan dosage forms and strengths|Dosage Forms and Strengths]]''' | |||
'''| [[Olmesartan contraindications|Contraindications]]''' | |||
'''| [[Olmesartan warnings and precautions|Warnings and Precautions]]''' | |||
'''| [[Olmesartan adverse reactions|Adverse Reactions]]''' | |||
'''| [[Olmesartan drug interactions|Drug Interactions]]''' | |||
'''| [[Olmesartan use in specific populations|Use in Specific Populations]]''' | |||
'''| [[Olmesartan overdosage|Overdosage]]''' | |||
'''| [[Olmesartan description|Description]]''' | |||
'''| [[Olmesartan clinical pharmacology|Clinical Pharmacology]]''' | |||
'''| [[Olmesartan nonclinical toxicology|Nonclinical Toxicology]]''' | |||
'''| [[Olmesartan clinical studies|Clinical Studies]]''' | |||
'''| [[Olmesartan how supplied storage and handling|How Supplied/Storage and Handling]]''' | |||
'''| [[Olmesartan patient counseling information|Patient Counseling Information]]''' | |||
'''| [[Olmesartan labels and packages|Labels and Packages]]''' | |||
==Mechanism of Action== | |||
[[Angiotensin]]II is formed from [[Angiotensin]]I in a reaction catalyzed by [[Angiotensin]]converting enzyme (ACE, kininase II). [[Angiotensin]]II is the principal pressor agent of the renin-[[Angiotensin]]system, 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 [[Angiotensin]]II by selectively blocking the binding of [[Angiotensin]]II to the AT1 receptor in vascular smooth muscle. Its action is, therefore, independent of the pathways for [[Angiotensin]]II 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-[[Angiotensin]]system with ACE inhibitors, which inhibit the biosynthesis of [[Angiotensin]]II from [[Angiotensin]]I, 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 [[Angiotensin]]II receptor inhibits the negative regulatory feedback of [[Angiotensin]]II on renin secretion, but the resulting increased plasma renin activity and circulating [[Angiotensin]]II levels do not overcome the effect of olmesartan on blood pressure. | |||
==References== | ==References== | ||
{{Reflist}} | |||
{{Angiotensin II receptor antagonists}} | {{Angiotensin II receptor antagonists}} | ||
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[[Category:Angiotensin II receptor antagonists]] | [[Category:Angiotensin II receptor antagonists]] | ||
[[Category:Imidazoles]] | [[Category:Imidazoles]] | ||
[[Category:Tetrazoles]] | |||
[[Category:Carboxylate esters]] | |||
[[Category:Alcohols]] | |||
[[Category:Biphenyls]] | |||
[[Category:Cardiovascular Drugs]] | |||
[[Category:Drugs]] | [[Category:Drugs]] | ||
Revision as of 20:04, 21 February 2014
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®
 |
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 for AngiotensinII 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.