Eprosartan: Difference between revisions
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{{Eprosartan}} | |||
{{CMG}}; {{AE}} {{SS}} | |||
'''''For patient information about Eprosartan, click [[Eprosartan (patient information)|here]].''''' | |||
{{SB}} TEVETEN<sup>®</sup> | |||
==Overview== | ==Overview== | ||
'''Eprosartan''' is an [[[[angiotensin]] II receptor antagonist]] used for the treatment of [[hypertension|high blood pressure]]. It is marketed as'''Teveten'''® by the [[Biovail Corporation]] in the United States and by [[Solvay (company)|Solvay Pharmaceuticals]] elsewhere. It is sometimes paired with [[hydrochlorothiazide]]. | |||
The drug acts on the [[renin-[[angiotensin]] system]] in two ways to decrease [[total peripheral resistance]]. First, it blocks the binding of[[[[angiotensin]] II]] to AT<sub>1</sub> receptors in vascular [[smooth muscle]], causing vascular dilatation. Second, it inhibits [[sympathetic nervous system|sympathetic]] [[norepinephrine]] production, further reducing blood pressure. | |||
== | As with other [[angiotensin]] II receptor antagonists, eprosartan is generally better tolerated than [[enalapril]] (an [[ACE inhibitor]]), especially among the elderly.<ref>{{cite journal |author=Ruilope L, Jäger B, Prichard B |title=Eprosartan versus enalapril in elderly patients with hypertension: a double-blind, randomized trial |journal=Blood Press. |volume=10 |issue=4 |pages=223-9 |year=2001 |pmid=11800061 |doi=}}</ref> | ||
< | ==Category== | ||
Category:[[angiotensin]] II receptor antagonists;Imidazoles;Thiophenes;Benzoic acids;Cardiovascular Drugs | |||
==FDA Package Insert== | |||
''' [[Eprosartan indications and usage|Indications and Usage]]''' | |||
'''| [[Eprosartan dosage and administration|Dosage and Administration]]''' | |||
'''| [[Eprosartan dosage forms and strengths|Dosage Forms and Strengths]]''' | |||
'''| [[Eprosartan contraindications|Contraindications]]''' | |||
'''| [[Eprosartan warnings and precautions|Warnings and Precautions]]''' | |||
'''| [[Eprosartan adverse reactions|Adverse Reactions]]''' | |||
'''| [[Eprosartan drug interactions|Drug Interactions]]''' | |||
'''| [[Eprosartan use in specific populations|Use in Specific Populations]]''' | |||
'''| [[Eprosartan overdosage|Overdosage]]''' | |||
'''| [[Eprosartan description|Description]]''' | |||
'''| [[Eprosartan clinical pharmacology|Clinical Pharmacology]]''' | |||
'''| [[Eprosartan nonclinical toxicology|Nonclinical Toxicology]]''' | |||
'''| [[Eprosartan clinical studies|Clinical Studies]]''' | |||
'''| [[Eprosartan how supplied storage and handling|How Supplied/Storage and Handling]]''' | |||
'''| [[Eprosartan patient counseling information|Patient Counseling Information]]''' | |||
'''| [[Eprosartan labels and packages|Labels and Packages]]''' | |||
==Mechanism of Action== | |||
[[angiotensin]]II (formed from [[angiotensin]]I in a reaction catalyzed by [[angiotensin]]-converting enzyme [kininase II]), a potent vasoconstrictor, is the principal pressor agent of the renin-[[angiotensin]]system. [[angiotensin]]II also stimulates aldosterone synthesis and secretion by the adrenal cortex, cardiac contraction, renal resorption of sodium, activity of the sympathetic nervous system, and smooth muscle cell growth. Eprosartan blocks the vasoconstrictor and aldosterone-secreting effects of [[angiotensin]]II by selectively blocking the binding of [[angiotensin]]II to the AT1 receptor found in many tissues (e.g., vascular smooth muscle, adrenal gland). There is also an AT2 receptor found in many tissues but it is not known to be associated with cardiovascular homeostasis. Eprosartan does not exhibit any partial agonist activity at the AT1 receptor. Its affinity for the AT1 receptor is 1,000 times greater than for the AT2 receptor. In vitro binding studies indicate that eprosartan is a reversible, competitive inhibitor of the AT1 receptor. | |||
Blockade of the AT1 receptor removes the negative feedback of [[angiotensin]]II on renin secretion, but the resulting increased plasma renin activity and circulating [[angiotensin]]II do not overcome the effect of eprosartan on blood pressure. | |||
TEVETEN® does not inhibit kininase II, the enzyme that converts [[angiotensin]]I to [[angiotensin]]II and degrades bradykinin; whether this has clinical relevance is not known. It does not bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation. | |||
==References== | |||
{{Reflist}} | |||
{{Angiotensin II receptor antagonists}} | {{Angiotensin II receptor antagonists}} | ||
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[[Category:Imidazoles]] | [[Category:Imidazoles]] | ||
[[Category:Thiophenes]] | [[Category:Thiophenes]] | ||
[[Category:Benzoic acids]] | |||
[[Category:Cardiovascular Drugs]] | |||
[[Category:Drugs]] | [[Category:Drugs]] | ||
Revision as of 14:52, 20 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 Eprosartan, click here.
Synonyms / Brand Names: TEVETEN®
Overview
Eprosartan is an [[angiotensin II receptor antagonist]] used for the treatment of high blood pressure. It is marketed asTeveten® by the Biovail Corporation in the United States and by Solvay Pharmaceuticals elsewhere. It is sometimes paired with hydrochlorothiazide.
The drug acts on the [[renin-angiotensin system]] in two ways to decrease total peripheral resistance. First, it blocks the binding of[[angiotensin II]] to AT1 receptors in vascular smooth muscle, causing vascular dilatation. Second, it inhibits sympathetic norepinephrine production, further reducing blood pressure.
As with other angiotensin II receptor antagonists, eprosartan is generally better tolerated than enalapril (an ACE inhibitor), especially among the elderly.[1]
Category
Category:angiotensin II receptor antagonists;Imidazoles;Thiophenes;Benzoic acids;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 (formed from angiotensinI in a reaction catalyzed by angiotensin-converting enzyme [kininase II]), a potent vasoconstrictor, is the principal pressor agent of the renin-angiotensinsystem. angiotensinII also stimulates aldosterone synthesis and secretion by the adrenal cortex, cardiac contraction, renal resorption of sodium, activity of the sympathetic nervous system, and smooth muscle cell growth. Eprosartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensinII by selectively blocking the binding of angiotensinII to the AT1 receptor found in many tissues (e.g., vascular smooth muscle, adrenal gland). There is also an AT2 receptor found in many tissues but it is not known to be associated with cardiovascular homeostasis. Eprosartan does not exhibit any partial agonist activity at the AT1 receptor. Its affinity for the AT1 receptor is 1,000 times greater than for the AT2 receptor. In vitro binding studies indicate that eprosartan is a reversible, competitive inhibitor of the AT1 receptor.
Blockade of the AT1 receptor removes the negative feedback of angiotensinII on renin secretion, but the resulting increased plasma renin activity and circulating angiotensinII do not overcome the effect of eprosartan on blood pressure.
TEVETEN® does not inhibit kininase II, the enzyme that converts angiotensinI to angiotensinII and degrades bradykinin; whether this has clinical relevance is not known. It does not bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation.