Telmisartan
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 Telmisartan, click here.
Synonyms / Brand Names: MICARDIS®
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Overview
Telmisartan (INN) /tɛlmɪˈsɑːrtən/ is an AngiotensinII receptor antagonist (Angiotensinreceptor blocker, ARB) used in the management of hypertension. It is marketed under the trade name Micardis (by Boehringer Ingelheim), among others.
Category
Category:AngiotensinII receptor antagonists;Benzimidazoles;Benzoic acids;Biphenyls;PPAR agonists;Category:Cardiovascular Drugs
FDA Package Insert
Indications and Usage | Dosage and Administration | 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 | Labels and Packages
Mechanism of Action
AngiotensinII is formed from AngiotensinI in a reaction catalyzed by angiotensin-converting 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. Telmisartan blocks the vasoconstrictor and aldosterone-secreting effects of AngiotensinII by selectively blocking the binding of AngiotensinII to the AT1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland. Its action is therefore independent of the pathways for AngiotensinII synthesis.
There is also an AT2 receptor found in many tissues, but AT2 is not known to be associated with cardiovascular homeostasis. Telmisartan has much greater affinity (>3,000 fold) 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 widely used in the treatment of hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Because telmisartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known. Telmisartan does not bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation.
Blockade of the AngiotensinII receptor inhibits the negative regulatory feedback of AngiotensinII on renin secretion, but the resulting increased plasma renin activity and AngiotensinII circulating levels do not overcome the effect of telmisartan on blood pressure.