Timisartan is a specific angiotensin II receptor (AT type I) antagonist. Telmisartan substitutes for the angiotensin II receptor by binding with high affinity to the AT I receptor subtype (a known angiotensin II site of action). Telmisartan does not have any site agonist effect at the AT I receptor site, and telmisartan selectively binds to the AT I receptor, a binding effect that is long-lasting. Telmisartan has no affinity for other receptors, including AT2 and other less well characterized AT receptors. The function of the other receptors mentioned above is not known, nor are the possible receptor overstimulation effects due to the increased angiotensin II levels caused by telmisartan. Telmisartan does not inhibit plasma renin or block ion channels in humans. Telmisartan does not inhibit angiotensin-converting enzyme II, which may also degrade bradykinin resulting in adverse effects due to increased bradykinin action. In humans, 80 mg of telmisartan almost completely inhibits angiotensin II-induced increases in blood pressure. The inhibitory effect lasts for 24 hours and is still measurable at 48 hours. The antihypertensive effect becomes progressively more pronounced within 3 hours after the first dose of timosartan. Maximum antihypertensive effect is obtained 4 weeks after the start of treatment and can be maintained during long-term therapy. Timosartan treatment, if abruptly interrupted, gradually returns blood pressure to pretreatment levels after several days without rebound hypertension. In clinical trial studies directly comparing the two hypertension medications, the incidence of dry cough was significantly lower in patients in the telmisartan-treated group than in the angiotensin-converting enzyme inhibitor-treated group.