Telmisartan is a non-peptide angiotensin-II receptor antagonist. Angiotensin-II is formed from angiotensin-I in a reaction catalyzed by angiotensin converting enzyme. Angiotensin-II is the principal 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. Telmisartan has much greater affinity (>3,000 fold) for the AT₁ receptor than for the AT₂ receptor. Because Telmisartan does not inhibit ACE (kininase-II), it does not affect the response to bradykinin. Telmisartan does not bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation.