Telstar 40/Telstar 80 Mechanism of Action

Pharmacology: Pharmacodynamics and Pharmacokinetics: Telmisartan is an orally active and specific angiotensin II receptor (type AT₁) antagonist. Telmisartan displaces angiotensin II with very high affinity from its binding site at the AT₁ receptor subtype, which is responsible for the known actions of angiotensin II. Telmisartan does not exhibit any partial agonist activity at the AT₁ receptor. Telmisartan selectively binds the AT₁ receptor. The binding is long-lasting. Telmisartan does not show affinity for other receptors, including AT₂ and other less characterised AT receptors. The functional role of these receptors is not known, nor is the effect of their possible overstimulation by angiotensin II, whose levels are increased by telmisartan. Plasma aldosterone levels are decreased by telmisartan. Telmisartan does not inhibit human plasma renin or block ion channels. Telmisartan does not inhibit angiotensin converting enzyme (kininase II), the enzyme which also degrades bradykinin. Therefore it is not expected to potentiate bradykinin-mediated adverse effects.
In human, an 80 mg dose of telmisartan almost completely inhibits the angiotensin II evoked blood pressure increase. The inhibitory effect is maintained over 24 hours and still measurable up to 48 hours.
Telmisartan is rapidly absorbed from the gastrointestinal tract, the absolute oral bioavailability is dose dependent and is about 42% after a 40 mg dose and 58% after a 160 mg dose. Peak plasma concentrations of telmisartan are reached about 0.5 to 1 hour after an oral dose. Telmisartan is over 99% bound to plasma proteins. It is excreted almost entirely in the faeces via bile, mainly as unchanged drug. The terminal half-life of telmisartan is about 24 hours.