It relaxes vascular smooth muscle, releases nitric oxide (NO) through metabolism to generate isosorbide mononitrate, activates guanylate cyclase to increase cyclic guanosine monophosphate (cGMP) in smooth muscle cells, thereby relaxing vascular smooth muscle, dilating peripheral arteries and veins, reducing myocardial oxygen consumption and increasing oxygen supply, and relieving angina pectoris.

This product was originally an antiviral drug. Its anti-Parkinson's disease mechanism is mainly to promote the synthesis and release of striatal dopamine, reduce the reuptake of dopamine by nerve cells, and have an anti-acetylcholine effect, thereby improving the symptoms of Parkinson's patients.

Anti-hormone drugs. The mechanism of ovulation stimulation of this product is not fully understood. Since this product has a weak excitatory and strong antagonistic effect on estrogen, ovulation stimulation may be in the hypothalamus. First, antagonism is dominant. By competitively occupying the hypothalamic estrogen receptors, it interferes with the negative feedback of endogenous estrogen, promotes the secretion of luteinizing hormone and follicle-stimulating hormone, and then stimulates the growth of follicles. After the follicles mature, the release of estrogen increases, and the release of preovulatory gonadotropin is stimulated by positive feedback to reach a peak, thus ovulation. The treatment of male infertility may be related to the increase of FSH and LH and the promotion of sperm production.

Aldosterone antagonist. It can inhibit the sodium retention, potassium excretion and water retention caused by the action of aldosterone on the distal renal tubule. When the blood aldosterone concentration is not high, the effect of this product is also weak. On the contrary, when secondary aldosterone increases, the effect of this drug is significant.

The chemical structure of this product is similar to that of haloperidol and pethidine, but the therapeutic dose has no effect on the central nervous system. The effect on intestinal smooth muscle is similar to that of opioids. It can inhibit the contraction of intestinal smooth muscle and reduce intestinal peristalsis. It can also reduce the release of acetylcholine from the nerve endings of the intestinal wall, and directly inhibit the peristaltic reflex through the local interaction of cholinergic and non-cholinergic neurons. This product can prolong the residence time of food in the small intestine, promote the absorption of water, electrolytes and glucose, and inhibit intestinal excessive secretion caused by prostaglandins, cholera toxin and other enterotoxins. In addition, this product can also increase the tension of the anal sphincter and inhibit fecal incontinence or urgency.