| Generic Name |
Valsartan Dispersible Tablets |
| Strength |
80mg |
| Packing |
7 Tablets/box |
| Origin |
China |
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Product name:
Valsartan Dispersible Tablets
Character:
This product is white.
Indications:
Treatment of mild and moderate essential hypertension.
Adverse reactions:
In rare cases, valsartan causes a decrease in hemoglobin and hematocrit. Controlled clinical trials found significant reductions in hemoglobin and hematocyte (]20% in the valsartan treatment group of 0.8% and 0.4%, respectively. In the placebo group, it was 0.1%.
Controlled clinical trials found neutropenia in 1.9% of valsartan treated patients and 1.6% of ACEI treated patients. Serum creatinine, serum potassium and total bilirubin were significantly increased by 0.8%, 4.4% and 6% in valsartan group, and 1.6%, 6.4% and 12.9% in ACEI group, respectively. Occasionally elevated liver function indicators were observed. When patients with essential hypertension are treated with valsartan, no special laboratory indicators need to be monitored.
Pharmacology and toxicology:
Action mechanism
The activator of the renin-angiotensin-aldosterone system (RAAS) is angiotensin II, which is formed by angiotensin I under the action of angiotensin-converting enzyme (ACE). Angiotensin II binds to specific receptors on cell membranes of various tissues. It has a variety of physiological effects, including direct or indirect involvement in blood pressure regulation. Angiotensin II is a powerful vasoconstricting substance, which has a direct pressor effect, and can also promote sodium reabsorption and stimulate aldosterone secretion.
Valsartan is an orally effective specific angiotensin (AT) receptor antagonist that selectively acts on the AT1 receptor subtype, producing all known effects. The AT2 receptor subtype was not associated with cardiovascular effects. Valsartan does not have any partial agonist activity on the AT1 receptor. Valsartan has a 20,000 times stronger affinity with the AT1 receptor than the AT2 receptor.
ACE converts angiotensin I to angiotensin II and degrades bradykinin. Angiotensin II receptor antagonist Valsartan has no inhibitory effect on ACE and does not cause bradykinin or substance P retention, so it does not cause cough. Clinical trials comparing valsartan with ACE inhibitors confirmed that the incidence of dry cough in valsartan group (2.6%) was significantly lower than that in ACE inhibitor group (7.9%)(P[0.05). In a clinical trial of patients who developed dry cough after receiving ACE inhibitors, 19.5%, 19.0%, and 68.5% of patients in the valsartan, diuretic, and ACEI groups developed cough, respectively (P<0.05). Valsartan has no effect on other hormone receptors or ion channels known to play an important role in cardiovascular regulation.
Drug effect
Valsartan lowers elevated blood pressure without affecting heart rate.
For most patients, a single dose of oral antihypertensive effect within 2 hours, 4-6 hours to reach the peak effect, the antihypertensive effect maintained until more than 24 hours after taking the drug. The maximum antihypertensive effect is achieved after 2-4 weeks of treatment and is maintained during long-term treatment. Combined with thiazide diuretics can further significantly enhance the antihypertensive effect.
Abrupt termination of valsartan treatment did not cause high blood pressure "rebound" or other side effects.
Valsartan did not affect total cholesterol, triglycerides, blood sugar, and uric acid levels in hypertensive patients.
Storage:Seal and store in a dry place (no more than 30ºC).
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