Lunan BETTER Pharmaceutical Co., Ltd.

Antihistamine effect

It is an orally effective specific angiotensin (AT) II receptor antagonist that selectively acts on the AT1 receptor subtype, with an affinity for the AT1 receptor 20,000 times stronger than that for the AT2 receptor. For most patients, a single oral dose produces a blood pressure lowering effect within 2 hours, reaches a peak effect within 4-6 hours, and the blood pressure lowering effect is maintained for more than 24 hours after taking the medicine. In long-term treatment, the maximum blood pressure lowering effect is achieved after 2-4 weeks of treatment and is maintained. The combined use with hydrochlorothiazide significantly enhances the antihypertensive effect of valsartan. Sudden termination of valsartan treatment does not cause hypertension "rebound" or other side effects. Valsartan does not affect the fasting total cholesterol, triglyceride, blood sugar or uric acid levels of hypertensive patients. Valsartan has no inhibitory effect on ACE, does not cause retention of bradykinin and substance P, and is therefore less likely to cause cough.

Inhibiting the co-transport of sodium and chloride ions and competing for chloride ion sites can affect the reabsorption of electrolytes, which will directly increase the excretion of sodium and chloride and indirectly reduce plasma volume, thereby increasing plasma renin activity, aldosterone secretion and potassium excretion, and reducing serum potassium. Because the renin-aldosterone system is angiotensin II-dependent, the combined use of angiotensin II receptor antagonists can reduce potassium loss associated with thiazide diuretics. The combined use of valsartan/hydrochlorothiazide has a clear antihypertensive effect and is more effective than the use of either drug alone.

Calcium antagonist, vasodilator. Inhibits transmembrane calcium ion influx of myocardial and vascular smooth muscle without changing blood calcium concentration, and has strong vascular selectivity. Dilates coronary vascular smooth muscle, reduces peripheral vascular resistance, increases cardiac ejection fraction and cardiac output, and does not change much in left ventricular end-diastolic pressure, increasing coronary blood flow.

Rosuvastatin is a selective and competitive HMG-CoA reductase inhibitor. It increases the number of liver LDL receptors on the cell surface, enhances the uptake and catabolism of LDL, inhibits liver VLDL synthesis, and reduces the total number of VLDL and LDL particles. It can reduce the levels of total cholesterol, LDL-C, ApoB, and non-HDL-C, while reducing TG and increasing HDL-C levels. For patients with hypertriglyceridemia, it can also reduce the levels of total cholesterol, LDL-C, VLDL-C, ApoB, non-HDL-C, and TG, and increase the level of HDL-C.

It inhibits the synthesis of bacterial proteins through the bacterial transpeptidation process and has antibacterial effects on a variety of Gram-positive aerobic bacteria, Gram-negative aerobic bacteria, anaerobic bacteria, sexually transmitted disease microorganisms and other microorganisms.