This product is a competitive angiotensin converting enzyme inhibitor, which prevents angiotensin I from being converted into angiotensin II, thereby reducing peripheral vascular resistance and reducing water and sodium retention by inhibiting aldosterone secretion. This product can also dilate peripheral blood vessels by interfering with the degradation of bradykinin. For patients with heart failure, this product can also reduce capillary wedge pressure and pulmonary vascular resistance, increase cardiac output and exercise tolerance time.

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

Selective α1 receptor blockers can reduce peripheral vascular resistance and have a lowering effect on both systolic and diastolic blood pressure; they have the effect of relaxing bladder and prostate smooth muscles and can relieve symptoms of dysuria caused by benign prostatic hypertrophy.

In acute toxicity experiments, the LD50 in mice and rats was greater than 4000 mg/Kg. In subacute toxicity experiments, Wistar male and female rats were given 40 mg, 200 mg and 1000 mg/Kg per day for 5 weeks, and male and female rabbits were given 6 mg, 60 mg and 600 mg/Kg per day for 23 consecutive days. There were no special changes in the blood, urine and morphological observations of the test animals. In chronic toxicity experiments, Wistar male and female rats were given 6 mg, 60 mg and 600 mg/Kg per day for 26 consecutive weeks. There were no special changes in the general state, blood and urine examinations, and morphological observations of the test animals.

Calcium ion antagonists, by regulating the influx of calcium ions on the cell membranes of myocardial conduction cells, myocardial contractile cells, and arterial smooth muscle cells, dilate coronary arteries, reduce myocardial oxygen consumption, slow down heart rate, lower blood pressure, and improve left ventricular diastolic function.