Valsartan Hydrochlorothiazide Tablets

Pharmacological action of valsartan Angiotensin I forms angiotensin II (AGII) under the action of angiotensin converting enzyme (ACE). AGII is an important active component of the renin-angiotensin-aldosterone system (RAAS). It binds to specific receptors on the cell membranes of various tissues and exerts a wide range of physiological effects, including direct or indirect participation in blood pressure regulation. Angiotensin II is a strong vasoconstrictor that can exert a direct pressor effect, promote sodium reabsorption, and stimulate aldosterone secretion. Valsartan is an orally effective specific angiotensin (AT) II receptor antagonist. It selectively acts on the AT1 receptor subtype, and its affinity for the AT1 receptor is 20,000 times stronger than that for the AT2 receptor. The AT1 receptor subtype mediates the physiological response of angiotensin II, and the AT2 receptor subtype is not related to cardiovascular effects. Valsartan has no partial agonist activity on the AT1 receptor. Valsartan does not inhibit ACE (also known as kininase II), which converts angiotensin I into angiotensin II and degrades bradykinin. Valsartan has no inhibitory effect on ACE and does not cause retention of bradykinin and substance P, so it is not easy to cause cough. Clinical trials comparing valsartan with ACE inhibitors have confirmed that the incidence of dry cough in the valsartan group (2.6%) is significantly lower than that in the ACE inhibitor group (7.9%) (P < 0.05). In a clinical trial of patients who had dry cough symptoms after receiving ACE inhibitor treatment, it was found that 19.5%, 19.0%, and 68.5% of patients in the valsartan group, diuretic group, and ACEI group had cough, respectively (P < 0.05). In clinical trials, the incidence of cough in patients treated with valsartan and hydrochlorothiazide was 2.9%. Valsartan has no effect on other hormone receptors or ion channels that are known to play an important role in cardiovascular regulation. Valsartan does not affect heart rate when lowering elevated blood pressure. For most patients, a single oral dose produces a hypotensive effect within 2 hours, reaches a peak effect within 4 to 6 hours, and the hypotensive effect is maintained for more than 24 hours after taking the medicine. In long-term treatment, the maximum antihypertensive effect is achieved after 2 to 4 weeks of treatment and is maintained. The antihypertensive effect of valsartan is significantly enhanced when used in combination with hydrochlorothiazide. Sudden termination of valsartan treatment does not cause rebound hypertension or other side effects. Valsartan does not affect fasting total cholesterol, triglycerides, blood sugar or uric acid levels in hypertensive patients. The main site of action of hydrochlorothiazide thiazide diuretics is the proximal end of the distal convoluted tubule. Studies have shown that there are high-affinity receptors in the renal cortex, which are the main binding site and site of action of thiazide diuretics, inhibiting the transport of sodium chloride in the proximal end of the distal convoluted tubule. The mode of action of thiazides is to inhibit the co-transport of sodium and chloride ions. Competing for the chloride ion site of action 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, concomitant use of angiotensin II receptor antagonists may reduce potassium losses associated with thiazide diuretics.

This product is a compound preparation. Each tablet contains 80 mg of valsartan and 12.5 mg of hydrochlorothiazide.

This product is a capsule, and the contents are white or off-white granules.

It is used to treat mild to moderate essential hypertension where blood pressure cannot be adequately controlled by a single drug. This product is not suitable for the initial treatment of hypertension.

Take one tablet each time, once a day, and the maximum antihypertensive effect can be achieved within 2-4 weeks of medication.

In two controlled clinical trials involving a total of 1570 patients, 730 patients received the combination of valsartan and hydrochlorothiazide, and the adverse events reported were as follows: Central nervous system Common (5%): headache (10.8%: placebo 17.2%), dizziness. Occasional (5-0.1%): fatigue, depression. Upper respiratory tract Occasional (5-0.1%): cough, rhinitis, sinusitis, pharyngitis, upper respiratory tract infection, epistaxis. Gastrointestinal tract Occasional (5-0.1%): nausea, diarrhea, indigestion, abdominal pain. Lower urinary tract Occasional (5-0.1%): frequent urination, urinary tract infection. Musculoskeletal system Occasional (5-0.1%): pain in the arms or legs, arthritis, myalgia, sprains and strains, muscle spasms. Other Occasional (5-0.1%): weakness, chest pain, asthenia, viral infection, visual disturbances, conjunctivitis. After the product entered the market, there have been some rare reports, including: angioedema, rash itching and other allergic reactions such as serum sickness, vasculitis, etc. Laboratory examinations showed that 5.8% of patients treated with the same product had a decrease in serum potassium of more than 20%, while the rate was 3.3% for patients receiving placebo. The following adverse events are related to the use of valsartan alone, but not to this product. In rare cases, valsartan causes a decrease in hemoglobin and hematocrit. Clinical controlled trials found that 0.8% and 0.4% of the valsartan treatment group had a significant decrease in hemoglobin and hematocrit (20%), respectively. The placebo group accounted for 0.1%. Clinical controlled trials found that the incidence of neutropenia in the valsartan group and ACEI group was 1.9% and 1.6%, respectively. The serum creatinine, blood potassium and total bilirubin in the valsartan group were significantly increased by 0.8%, 4.4% and 6%, respectively, and in the ACEI group by 1.6%, 6.4% and 12.9%, respectively. Occasionally, liver function indicators were elevated. For patients with essential hypertension receiving valsartan treatment, no special monitoring of laboratory indicators is required. Other adverse events reported in clinical trials of valsartan are: Occasionally (5-0.1%): arthralgia, gastroenteritis, neuralgia. Only one case of angioedema was reported. No causal relationship with valsartan treatment has been proven. Hydrochlorothiazide In patients receiving a single thiazide diuretic (including hydrochlorothiazide), the adverse reactions reported are as follows, and most patients use doses higher than those in this product: Electrolyte and metabolic disorders (see [Precautions]) Common (5%): hypokalemia. Occasionally (5-0.1%): hyponatremia, hypomagnesemia and hyperuricemia. Rarely (0.1%): hypercalcemia, increased blood sugar, glucosuria and worsening of diabetes. Very rare: hypochloremic alkalosis. Occasionally (5-0.1%): urticaria and other types of rashes. Rare (0.1%): photosensitivity. Very rare: necrotizing vasculitis, acute toxic epidermolysis, lupus erythematosus-like reaction, relapse of cutaneous lupus erythematosus. Gastrointestinal tract Occasional (5-0.1%): loss of appetite, mild nausea and vomiting. Rare (0.1%): abdominal symptoms, constipation, diarrhea, gastrointestinal symptoms. Very rare: pancreatitis. Liver Rare (0.1%): intrahepatic cholestasis or jaundice. Cardiovascular system Occasional (5-0.1%): orthostatic hypotension, alcohol, anesthetics or sedatives may aggravate it. Rare (0.1%): arrhythmia. Central nervous system Rare (0.1%): headache, dizziness or photo-headache, sleep disturbance, depression, paresthesia. Visual disturbances of the sense organs, especially in the first few weeks of treatment. Blood Rare (0.1%): thrombocytopenia, occasionally with purpura. Very rare: leukopenia, granulocytopenia, bone marrow suppression, hemolytic anemia. Other rare (5-0.1%): impotence. Very rare: allergic reactions, respiratory symptoms including pneumonia and pulmonary edema

Hypersensitivity to any of the ingredients in this product or to sulfonamide derivatives. Pregnancy (see [Use in Pregnant and Lactating Women]) Severe liver failure, biliary cirrhosis or cholestasis. Severe renal failure (creatinine clearance 30ml/min) or anuria. Refractory hypokalemia, hyponatremia or hypercalcemia and symptomatic hyperuricemia (history of gout or uric acid stones).

Precautions for children: Not yet clear. Precautions for pregnancy and lactation: Not for use by pregnant women. Precautions for the elderly: Not yet clear.

The antihypertensive effect of this product can be enhanced by co-administration with other antihypertensive drugs. It is necessary to be cautious and monitor the serum potassium level when co-administered with potassium-sparing diuretics, potassium supplements or potassium-containing salt substitutes, or other drugs that increase serum potassium (such as heparin). It has been reported that the simultaneous use of lithium, ACE inhibitors and/or thiazide diuretics can cause a reversible increase in serum potassium concentration and lithium poisoning. There is no experience of the simultaneous use of valsartan and lithium. Therefore, it is recommended to regularly monitor serum lithium levels when lithium and this product are used in combination. No clinically significant interactions have been observed between valsartan alone and any of the following drugs, including: cimetidine, warfarin, furosemide, digoxin, atenolol, indomethacin, hydrochlorothiazide, amlodipine and glibenclamide. Because this product contains thiazide diuretic components, the following interactions may occur: Co-administration with nonsteroidal anti-inflammatory drugs (such as salicylic acid derivatives, indomethacin) may weaken the diuretic and antihypertensive activity of the thiazide components in this product. Acute renal failure may occur if volume depletion is present. Concomitant administration with potassium-wasting diuretics (e.g. furosemide), corticosteroids, adrenocorticotropic hormone (ACTH), amphotericin B, carbenoxolone, penicillin G, or salicylic acid derivatives may exacerbate potassium and/or magnesium loss. Hypokalemia or hypomagnesemia caused by thiazides may increase the risk of arrhythmias in patients taking cardiac glycosides. Thiazide diuretics increase the effect of curare-like muscle relaxants. Adjustment of the dose of insulin or oral antidiabetic drugs may be necessary. Concomitant use with thiazide diuretics may increase the incidence of hypersensitivity reactions to allopurinol. May increase the risk of adverse reactions caused by amantadine. Thiazides may also enhance the blood glucose-raising effect of diazoxide. Thiazides may reduce the renal excretion of cytotoxic drugs (e.g. cyclophosphamide, methotrexate), thereby increasing their bone marrow suppressive effects. The bioavailability of thiazide diuretics may increase when anticholinergic drugs (e.g., atropine, biperiden) are given simultaneously, probably as a result of decreased gastrointestinal motility and slower gastric emptying. There are isolated reports of hemolytic anemia caused by the combined use of hydrochlorothiazide and methyldopa. Cholestyramine and colestipol reduce the absorption of thiazide diuretics. The combined use of thiazide diuretics and vitamin D or calcium salts can enhance the effect of raising blood calcium. The combined use of cyclosporine may increase the risk of hyperuricemia causing symptoms of gout.

Sealed and stored in a cool place.

Valsartan 80.0mg/ Hydrochlorothiazide 12.5mg

36 months

Lunan BETTER Pharmaceutical Co., Ltd.

• Founded in:

  2003-12-16

• Address:

  No. 209, Hongqi Road, Linyi City

• Tax NO.:

  91371300756399007K

• Registered Funds:

  115 million yuan

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