Reduce peripheral vascular resistance, increase cardiac output, reduce venous pressure, activate fibrinolysis, reduce fibrinogen levels, prevent platelet aggregation, promote the synthesis of pyrimidine nucleosides (NAD and NADP), increase the concentration of adenine nucleosides (AMP, ADP and ATP), hinder lipolysis, and reduce elevated cholesterol and triglyceride levels

Rifampicin is a semi-synthetic broad-spectrum antibacterial drug of the rifamycin class, which has antibacterial activity against a variety of pathogenic microorganisms. The drug has a significant bactericidal effect on Mycobacterium tuberculosis and some non-tuberculous mycobacteria (including Mycobacterium leprae, etc.) both inside and outside the host cells. Rifampicin has a good antibacterial effect on aerobic Gram-positive bacteria, including enzyme-producing strains of Staphylococcus aureus and methicillin-resistant strains, Streptococcus pneumoniae, other Streptococcus, Enterococcus, Listeria, Bacillus anthracis, Clostridium perfringens, Corynebacterium diphtheriae, anaerobic cocci, etc. It also has a high degree of antibacterial activity against aerobic Gram-negative bacteria such as Neisseria meningitidis, Haemophilus influenzae, and Neisseria gonorrhoeae. Rifampicin also has a good effect on Legionella, and has an inhibitory effect on pathogens such as Chlamydia trachomatis, lymphogranuloma venereum, and psittacosis.

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.

Selective postsynaptic a1 receptor blockers can relax vascular smooth muscle, dilate peripheral blood vessels, reduce peripheral vascular resistance, and lower blood pressure; dilate arteries and veins, reduce cardiac preload and afterload, and improve cardiac function; have little effect on renal blood flow and glomerular filtration rate, and can reduce urination difficulties in patients with prostatic hyperplasia by blocking a1 receptors in the bladder neck, prostate capsule and glands, and urethra; do not affect a2 receptors, rarely cause reflex tachycardia when lowering blood pressure, have little effect on cardiac output, and do not increase renin secretion. Long-term use has no effect on lipid metabolism.

Not clearly stated