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Revision as of 20:52, 1 July 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.