By protecting the energy metabolism of cells under hypoxia or ischemia, preventing the decrease of intracellular ATP levels, it ensures the normal function of ion pumps and the normal operation of transmembrane sodium-potassium flow, and maintains the stability of the intracellular environment. It helps maintain the energy metabolism of the heart and nerve sensory organs under ischemia and hypoxia, reduces intracellular acidosis and changes in transmembrane ion flow caused by ischemia, reduces the movement and infiltration of multinuclear neutrophils during ischemia and myocardial reperfusion, and reduces the scope of experimental infarction. While producing this effect, it has no significant effect on hemodynamics. It increases coronary blood flow reserve, delays the occurrence of exercise-induced ischemia, limits rapid fluctuations in blood pressure without significant changes in heart rate, reduces the frequency of angina attacks, and reduces the use of glyceryl trinitrate.

This drug is a hypoglycemic sulfonylurea-oral diabetes treatment drug. Gliclazide lowers blood sugar levels by stimulating pancreatic β cells to secrete insulin. For type 2 diabetes, gliclazide can restore the first-phase insulin secretion peak in response to glucose and increase the second-phase insulin secretion. It can be seen that the insulin secretion response induced or stimulated by glucose after a meal is significantly increased.

It is a sulfonamide diuretic that works by inhibiting the reabsorption of water and electrolytes in the dilution segment of the distal renal tubular cortex. The antihypertensive mechanism may include regulating calcium influx into vascular smooth muscle cells; stimulating the synthesis of prostaglandins PGE2 and prostaglandins PGI2; reducing the hypersensitivity of blood vessels to vasopressors, thereby inhibiting vasoconstriction. This product has little or no effect on cardiac output, heart rate and rhythm when lowering blood pressure. Long-term use of this product rarely affects glomerular filtration rate or renal blood flow. This drug does not affect the metabolism of blood lipids and carbohydrates.

It is a sulfonamide diuretic that works by inhibiting the reabsorption of water and electrolytes in the dilution segment of the distal renal tubular cortex. The antihypertensive mechanism may include regulating calcium influx into vascular smooth muscle cells; stimulating the synthesis of prostaglandins PGE2 and prostaglandins PGI2; reducing the hypersensitivity of blood vessels to vasopressors, thereby inhibiting vasoconstriction. This product has little or no effect on cardiac output, heart rate and rhythm when lowering blood pressure. Long-term use of this product rarely affects glomerular filtration rate or renal blood flow. This drug does not affect the metabolism of blood lipids and carbohydrates.

It is a sulfonamide diuretic that works by inhibiting the reabsorption of water and electrolytes in the dilution segment of the distal renal tubular cortex. The antihypertensive mechanism may include regulating calcium influx into vascular smooth muscle cells; stimulating the synthesis of prostaglandins PGE2 and prostaglandins PGI2; reducing the hypersensitivity of blood vessels to vasopressors, thereby inhibiting vasoconstriction. This product has little or no effect on cardiac output, heart rate and rhythm when lowering blood pressure. Long-term use of this product rarely affects glomerular filtration rate or renal blood flow. This drug does not affect the metabolism of blood lipids and carbohydrates.