It combines with adenosine triphosphate to form vitamin B1 pyrophosphate (thiamine diphosphate, cocarboxylase), which is a coenzyme necessary for carbohydrate metabolism; it can inhibit the activity of cholinesterase. When it is deficient, cholinesterase activity is enhanced, acetylcholine hydrolysis is accelerated, causing nerve impulse conduction disorders and affecting gastrointestinal and myocardial function.

This product is a carbonic anhydrase inhibitor that can inhibit the production of aqueous humor and reduce intraocular pressure. Acetazolamide can inhibit the activity of carbonic anhydrase in the ciliary epithelium, thereby reducing the production of aqueous humor (50% to 60%) and lowering intraocular pressure.

It is converted into flavin mononucleotide and flavin adenine dinucleotide, both of which are important coenzymes for tissue respiration. It can also activate vitamin B6, convert tryptophan into niacin, and may be involved in maintaining the integrity of red blood cells.

This product mainly acts on alpha receptors, directly stimulating alpha receptors. Its effect is weaker than that of norepinephrine but more persistent. Its cardiovascular effect is similar to that of norepinephrine. It can constrict blood vessels, continuously increase systolic and diastolic blood pressure, and enhance myocardial contractility. The cardiac output of normal people does not change much, but it can increase the cardiac output of patients with shock. The excitement of heart rate is not very significant, rarely causes arrhythmia, and has no central nervous system excitation effect. Because its pressor effect is reliable and lasts for a long time, it rarely causes reactions such as palpitations or decreased urine volume. When administered continuously, because this product indirectly replaces the transmitter in the adrenergic nerve vesicles, it can reduce the transmitter and weaken the intrinsic effect. Therefore, it should not be stopped suddenly to avoid rebound hypotension.