The following drug information is obtained from various newswires, published
medical journal articles, and medical conference presentations.
Treatment for hypertension. It may be used alone or in
combination with other antihypertensive agents.
Micardis has been evaluated for safety in more than 3700
patients, including 1900 treated for over six months and more than
1300 for over one year. Adverse experiences have generally been
mild and transient in nature and have only infrequently required
discontinuation of therapy.
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.
Telmisartan blocks the vasoconstrictor and aldosterone-secreting
effects of angiotensin II by selectively blocking the binding of
angiotensin II to the AT 1 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 AT 2 receptor found in many tissues, but AT 2 is
not known to be associated with cardiovascular homeostasis.
Telmisartan has much greater affinity (>3,000 fold) for the AT 1
receptor than for the AT 2 receptor. 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.