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Mechanism of Action - Antihypertensive ARBs — Micardis® (Telmisartan) Tablets

MICARDIS Mechanism of Action — Antihypertensive ARB

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. Telmisartan blocks the vasoconstrictor and aldosterone secreting effects of angiotensin II by selectively blocking the binding of angiotensin II 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 angiotensin II 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.

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Blockade of the renin-angiotensin system with ACE inhibitors, which inhibit the biosynthesis of angiotensin II from angiotensin I, 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 angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increased plasma renin activity and angiotensin II circulating levels do not overcome the effect of telmisartan on blood pressure.
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* Only Micardis® (telmisartan) 80-mg Tablets are indicated for cardiovascular risk reduction. All other MICARDIS and Micardis® HCT (telmisartan and hydrochlorothiazide) Tablets dosages are indicated for the treatment of hypertension only. MICARDIS 80 mg is indicated for reduction of the risk of myocardial infarction, stroke, or death from cardiovascular causes in patients 55 years of age or older at high risk of developing major cardiovascular events who are unable to take ACE inhibitors. High risk for cardiovascular events can be evidenced by a history of coronary artery disease, peripheral arterial disease, stroke, transient ischemic attack or high-risk diabetes (insulin-dependent or non-insulin-dependent) with evidence of end-organ damage. MICARDIS can be used in addition to other needed treatment (such as antihypertensive, antiplatelet or lipid-lowering therapy). Studies of telmisartan in this setting do not exclude that it may not preserve a meaningful fraction of the effect of the ACE inhibitor to which it was compared. Consider using the ACE inhibitor first, and, if it is stopped for cough only, consider re-trying the ACE inhibitor after the cough resolves. Use of telmisartan with an ACE inhibitor is not recommended.1

† Dosage must be individualized. In the treatment of hypertension, the usual starting dose of MICARDIS Tablets is 40 mg once a day. Blood pressure response is dose-related over the range of 20-80 mg. For patients who need even greater efficacy, MICARDIS HCT is available in 40/12.5-mg, 80/12.5-mg, and 80/25-mg tablets. Available as a unit dose. In the treatment of cardiovascular risk reduction, the recommended dose of MICARDIS is 80 mg once a day. It is not known whether doses lower than 80 mg of telmisartan are effective in reducing the risk of cardiovascular morbidity and mortality. When initiating MICARDIS therapy for cardiovascular risk reduction, monitoring of blood pressure is recommended and, if appropriate, adjustment of medications that lower blood pressure may be necessary.1


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