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 has a significant effect of increasing the number of peripheral blood leukocytes in normal rabbits. The peak value of leukocyte count occurs on the 4th day after the first administration, which is 72% higher than that before administration, which is better than the leukocyte-increasing drug shark liver alcohol. It has a significant effect of increasing leukocytes in rabbits induced by cobalt 60-gamma ray and deep X-ray irradiation. It also has a preventive effect on leukocyte decrease when administered two days before irradiation. It can prevent leukopenia in mice caused by mitomycin C. It has a synergistic inhibitory effect on the solid type of Ehrlich carcinoma when used in combination with cyclophosphamide, and the toxicity of leukocyte decrease caused by cyclophosphamide is significantly reduced.

Nicotinic acid is converted into nicotinamide in the body, and then combined with riboadenin to form nicotinamide adenine dinucleotide (coenzyme I) and nicotinamide adenine dinucleotide phosphate (coenzyme II), which are necessary for lipid amino acid, protein, purine metabolism, tissue respiration oxidation and glycogenolysis. Nicotinic acid can reduce the utilization of coenzyme A; by inhibiting the synthesis of very low density lipoprotein (VLDL), it affects the transport of cholesterol in the blood. Large doses can reduce serum cholesterol and triglyceride concentrations. Nicotinic acid has a peripheral vasodilation effect.

Nicotinic acid is converted into nicotinamide in the body, and then combined with riboadenin to form nicotinamide adenine dinucleotide (coenzyme I) and nicotinamide adenine dinucleotide phosphate (coenzyme II), which are necessary for lipid amino acid, protein, purine metabolism, tissue respiration oxidation and glycogenolysis. Nicotinic acid can reduce the utilization of coenzyme A; by inhibiting the synthesis of very low density lipoprotein (VLDL), it affects the transport of cholesterol in the blood. Large doses can reduce serum cholesterol and triglyceride concentrations. Nicotinic acid has a peripheral vasodilation effect.

No specific pharmacological information is provided