This product is an angiotensin II receptor antagonist. This product can selectively act on the AT1 receptor subtype known to be related to the action of angiotensin II, selectively block the binding of angiotensin II to the AT1 receptor of tissue cells such as the adrenal glands and vascular smooth muscle, inhibit vasoconstriction and aldosterone secretion, and produce a hypotensive effect. The affinity of this product for AT1 receptors is about 20,000 times higher than that for AT2 receptors. This product does not affect the action of bradykinin and ion channel function, nor does it bind to the receptors of other hormones that play an important regulatory role in cardiovascular function. This product has no carcinogenic, teratogenic, mutagenic toxicity, and no reproductive toxicity.

A specific angiotensin (AT) II receptor antagonist that selectively acts on the AT1 receptor subtype without affecting heart rate. A single oral dose produces a hypotensive effect within 2 hours, and combined use with hydrochlorothiazide significantly enhances the hypotensive effect.

Thiazide diuretics inhibit sodium chloride transport in the proximal distal convoluted tubule, increase sodium and chloride excretion, and reduce plasma volume. Combined use of angiotensin II receptor antagonists can reduce potassium loss.

A selective β1-adrenergic receptor blocker with no membrane stabilizing effect and endogenous sympathomimetic activity. However, it does not inhibit the bronchodilator effect of isoproterenol. Its mechanism of lowering blood pressure and reducing myocardial oxygen consumption is the same as that of propranolol. Large-scale clinical trials have confirmed that atenolol can reduce the mortality rate of acute myocardial infarction within 0 to 7 days. The therapeutic dose has no significant inhibition on myocardial contractility.

It is a selective beta-1 adrenergic receptor blocker with no membrane stabilizing effect and endogenous sympathomimetic activity. However, it does not inhibit the bronchodilator effect of isoproterenol. Its mechanism of lowering blood pressure and reducing myocardial oxygen consumption is the same as that of propranolol. Large-scale clinical trials have confirmed that atenolol can reduce the mortality rate of acute myocardial infarction within 0 to 7 days. The therapeutic dose has no significant inhibition on myocardial contractility.

It has a significant bactericidal effect on Mycobacterium tuberculosis and some non-tuberculous mycobacteria (including Mycobacterium leprae, etc.) both inside and outside the host cells. It firmly binds to the beta subunit of the DNA-dependent RNA polymerase, inhibits the synthesis of bacterial RNA, prevents the enzyme from connecting to DNA, thereby blocking the RNA transcription process and stopping the synthesis of DNA and protein.

It has a highly selective bactericidal effect on all types of Mycobacterium tuberculosis, with a strong effect on Mycobacterium tuberculosis in the growth and reproduction stage, and a weaker and slower effect on Mycobacterium tuberculosis in the dormant stage. The mechanism of action may be to inhibit the synthesis of mycolic acid in sensitive bacteria and cause the cell wall to rupture.

It has a significant bactericidal effect on Mycobacterium tuberculosis and some non-tuberculous mycobacteria (including Mycobacterium leprae, etc.) both inside and outside the host cells. It firmly binds to the beta subunit of the DNA-dependent RNA polymerase, inhibits the synthesis of bacterial RNA, prevents the enzyme from connecting to DNA, thereby blocking the RNA transcription process and stopping the synthesis of DNA and protein.

It has a highly selective bactericidal effect on all types of Mycobacterium tuberculosis, with a strong effect on Mycobacterium tuberculosis in the growth and reproduction stage, and a weaker and slower effect on Mycobacterium tuberculosis in the dormant stage. The mechanism of action may be to inhibit the synthesis of mycolic acid in sensitive bacteria and cause the cell wall to rupture.