Pharmacology and toxicology of telmisartan

Telmisartan is an orally effective, specific angiotensin II receptor (AT1 type) antagonist. It binds with high affinity to the angiotensin II receptor AT1 subtype (known angiotensin II action site). The binding effect is long-lasting. But there was no partial excitation dose effect. Due to the increased levels of angiotensin II caused by telmisartan, it is also unknown whether there may be a straightforward receptor overstimulation effect. Telmisartan does not inhibit human whole plasma renin and does not block ion channels. Angiotensin transferase (Kin II) can also release bradykinin, and since telmisartan does not inhibit angiotensin converting enzyme, there will be no adverse reactions caused by the enhanced effect of bradykinin. Telmisartan has no affinity for other receptors, including AT2 and other AT receptors with fewer features, and its function is still unclear.
In the human body, administering 80mg of telmisartan can almost completely inhibit the increase in blood pressure caused by angiotensin II, and the inhibitory effect lasts for 24 hours, which can still be measured at 48 hours.
The antihypertensive effect gradually became apparent within 3 hours after the first dose of telmisartan. The maximum antihypertensive effect can be achieved 4 weeks after the start of treatment and can be maintained over the long term.
The dosage used in preclinical safety studies is equivalent to the clinical treatment dosage and can cause a decrease in red blood cell index (red blood cell, hemoglobin, hematocrit), changes in renal hemodynamics (increase in blood urea nitrogen and creatinine), and an increase in blood potassium in animals with normal blood pressure. Dilation and atrophy of renal tubules can be seen in dogs. Gastrointestinal mucosal damage (erosion, ulcer, or inflammation) can also be seen in rats and dogs. These pharmacological adverse reactions, known from preclinical studies, are common reactions between angiotensin converting enzyme inhibitors and angiotensin II antagonists, and can be prevented using oral salt supplements.