Because telmisartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin.
ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Truetel has a much greater affinity ( > 3,000 fold) for the AT1 receptor than for the AT2 receptor.īlockade 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. There is also an AT2 receptor found in many tissues, but AT2 is not known to be associated with cardiovascular homeostasis. Its action is therefore independent of the pathways for angiotensin II synthesis.
Truetel 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. 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. Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II).
