Pharmaceutical Medicines

Approx. Rs 24 / Pack(s) Get Latest Price

Mechanism of Action:

Atenolol competes with sympathomimetic neurotransmitters such as catecholamines for binding at beta (1)-adrenergic receptors in the heart and vascular smooth muscle, inhibiting sympathetic stimulation. This results in a reduction in resting heart rate, cardiac output, systolic and diastolic blood pressure, and reflex orthostatic hypotension. Higher doses of atenolol also competitively block beta (2)-adrenergic responses in the bronchial and vascular smooth muscles.

Approx. Rs 55 / Pack Get Latest Price

Mechanism of Action:

• Atorvastatin Calcium is a selective, competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3methylglutaryl-coenzyme A to mevalonate, a precursor of sterols, including cholesterol. Cholesterol and triglycerides circulate in the bloodstream as part of lipoprotein complexes. With ultracentrifugation, these complexes separate into HDL (high-density lipoprotein), IDL (intermediate-density lipoprotein), LDL (low-density lipoprotein), and VLDL (very-low-density lipoprotein) fractions. Triglycerides (TG) and cholesterol in the liver are incorporated into VLDL and released into the plasma for delivery to peripheral tissues. LDL is formed from VLDL and is catabolized primarily through the high-affinity LDL receptor. Clinical and pathologic studies show that elevated plasma levels of total cholesterol (total-C), LDL-cholesterol (LDL-C), and apolipoprotein B (apo B) promote human atherosclerosis and are risk factors for developing cardiovascular disease, while increased levels of HDL-C are associated with a decreased cardiovascular risk
• In animal models, Atorvastatin Calcium lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the cell surface to enhance uptake and catabolism of LDL; Atorvastatin Calcium also reduces LDL production and the number of LDL particles. Atorvastatin Calcium reduces LDL-C in some patients with homozygous familial hypercholesterolemia (FH), a population that rarely responds to other lipid-lowering medication(s).
• A variety of clinical studies have demonstrated that elevated levels of total-C, LDL-C, and apo B (a membrane complex for LDL-C) promote human atherosclerosis. Similarly, decreased levels of HDL-C (and its transport complex, apo A) are associated with the development of atherosclerosis. Epidemiologic investigations have established that cardiovascular morbidity and mortality vary directly with the level of total-C and LDL-C, and inversely with the level of HDL-C
• Atorvastatin Calcium reduces total-C, LDL-C, and apo B in patients with homozygous and heterozygous FH, nonfamilial forms of hypercholesterolemia, and mixed dyslipidemia. Atorvastatin Calcium also reduces VLDL-C and TG and produces variable increases in HDL-C and apolipoprotein A-1. Atorvastatin Calcium reduces total-C, LDL-C, VLDL-C, apo B, TG, and non-HDL-C, and increases HDL-C in patients with isolated hypertriglyceridemia. Atorvastatin Calcium reduces intermediate density lipoprotein cholesterol (IDL-C) in patients with dysbetalipoproteinemia.
• Like LDL, cholesterol-enriched triglyceride-rich lipoproteins, including VLDL, intermediate density lipoprotein (IDL), and remnants, can also promote atherosclerosis. Elevated plasma triglycerides are frequently found in a triad with low HDL-C levels and small LDL particles, as well as in association with non-lipid metabolic risk factors for coronary heart disease. As such, total plasma TG has not consistently been shown to be an independent risk factor for CHD. Furthermore, the independent effect of raising HDL or lowering TG on the risk of coronary and cardiovascular morbidity and mortality has not been determined.

Approx. Rs 50 / Pack Get Latest Price

Mechanism of Action:

Angiotensin II [formed from angiotensin I in a reaction catalyzed by angiotensin converting enzyme (ACE, kininase II)], is a potent vasoconstrictor, the primary vasoactive hormone of the renin-angiotensin system and an important component in the pathophysiology of hypertension. It also stimulates aldosterone secretion by the adrenal cortex. Losartan and its principal active metabolite block the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor found in many tissues, (e.g., vascular smooth muscle, adrenal gland). There is also an AT2 receptor found in many tissues but it is not known to be associated with cardiovascular homeostasis. Both Losartan and its principal active metabolite do not exhibit any partial agonist activity at the AT1 receptor and have much greater affinity (about 1000-fold) for the AT1 receptor than for the AT2 receptor. In vitro binding studies indicate that Losartan is a reversible, competitive inhibitor of the AT1 receptor. The active metabolite is 10 to 40 times more potent by weight than Losartan and appears to be a reversible, non-competitive inhibitor of the AT1 receptor.Neither Losartan nor its active metabolite inhibits ACE (kininase II, the enzyme that converts angiotensin I to angiotensin II and degrades bradykinin); nor do they bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation.

Approx. Rs 66.75 / Pack Get Latest Price

Mechanism of Action:

• Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Telmisartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland. Its action is therefore independent of the pathways for angiotensin II synthesis.
• There is also an AT2 receptor found in many tissues, but AT2 is not known to be associated with cardiovascular homeostasis. Telmisartan has much greater affinity (> 3, 000 fold) for the AT1 receptor than for the AT2 receptor.
• Blockade of the renin-angiotensin system with ACE inhibitors, which inhibit the biosynthesis of angiotensin II from angiotensin I, is widely used in the treatment of hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Because telmisartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known. Telmisartan does not bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation.
• Blockade of the angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increased plasma renin activity and angiotensin II circulating levels do not overcome the effect of telmisartan on blood pressure.

Approx. Rs 465 / Strip Get Latest Price

Piracetam:

• Piracetam, the prototype of the so-called "nootropic drugs" is used since many years in different countries to treat cognitive impairment in aging and dementia. Piracetam has been shown to alter the physical properties of the plasma membrane by increasing its fluidity and by protecting the cell against hypoxia. It increases red cell deformability and normalizes aggregation of hyperactive platelets. Piracetam is an agent with antithrombotic, neuroprotective and rheological properties. Treatment with piracetam improves learning, memory, brain metabolism, and capacity. The drug influences neuronal and vascular functions and influences cognitive function without acting as a or stimulant.

 

Citicoline:

• Citicoline activates biosynthesis of structural phospholipids of neuronal membranes, increases brain metabolism, and acts upon the levels of different neurotransmitters. A number of therapeutic actions of citicoline are indicated which are as follows:A neuroprotective effect in hypoxic and ischemic conditions, decreasing the volume of ischemic lesionImproves learning and memory performance in animal models of brain agingRestores the activity of mitochondrial ATPase and membrane Na+/K+ATPaseInhibits activation of certain phospholipases and accelerates reabsorption of cerebral edemaInhibits mechanisms of apoptosis associated to cerebral ischemia.

Approx. Rs 36 / Pack Get Latest Price

Mechanism of Action:

• Glimepiride is a sulphonylurea antihyperglycemic agent that may be given in a single daily dose. It acts by stimulating insulin release from pancreatic beta-cells and possibly also via extrapancreatic mechanisms. The major site of activity of Glimepiride is thought to be membrane receptors on pancreatic beta-cells, where it acts via ATP-regulated potassium (KATP) channels, resulting in membrane depolarisation and release of insulin. Glimepiride is also internalised into pancreatic beta-cells, where it associates with secretory granules. This internalisation is thought to reflect insulinotropic mechanisms of Glimepiride other than at potassium channels. Glimepiride decreases blood glucose and increases blood insulin levels, with maximum effects during the first 4 hours after the dose.

Approx. Rs 22 / Pack Get Latest Price

We offer the qualitative range of Vizicip 250 and 500mg Tablet to our valuable patrons. The provided tablet fights bacteria in the body highly admired by our clients due to its exact composition. This tablet is processed under the stern surveillance of adept workforce using high grade chemical compounds and contemporary technology. Furthermore, to ensure its quality, this tablet is rigorously examined against numerous quality parameters in adherence to defined medical industry standards.

Features:

• Free from harmful chemical compounds
• Safe to use
• Exact composition

Approx. Rs 189.28 / Strip Get Latest Price

Mechanism of Action:

• Amoxicillin exerts a bactericidal action against sensitive organisms during the stage of active multiplication through the inhibition of the biosynthesis of bacterial cell wall mucopeptides. Clavulanic acid inhibits specific β-lactamases of some microorganisms and allows amoxicillin to inhibit amoxicillin (ampicillin) resistant organisms which produce clavulanic acid sensitive β-lactamases

Approx. Rs 70 / Pack Get Latest Price

Mechanism of Action:

Amlodipine is a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker) that inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle. Experimental data suggest that amlodipine binds to both dihydropyridine and nondihydropyridine binding sites. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Amlodipine inhibits calcium ion influx across cell membranes selectively, with a greater effect on vascular smooth muscle cells than on cardiac muscle cells. Negative inotropic effects can be detected in vitro but such effects have not been seen in intact animals at therapeutic doses. Serum calcium concentration is not affected by amlodipine. Within the physiologic pH range, amlodipine is an ionized compound (pKa=8.6), and its kinetic interaction with the calcium channel receptor is characterized by a gradual rate of association and dissociation with the receptor binding site, resulting in a gradual onset of effect.Amlodipine is a peripheral arterial vasodilator that acts directly on vascular smooth muscle to cause a reduction in peripheral vascular resistance and reduction in blood pressure.

Approx. Rs 95 / Pack Get Latest Price

After oral administration, Atorvastatin is rapidly absorbed, with peak serum concentrations reaching within 1 to 2 hours. Extent of absorption increases in proportion to Atorvastatin dose. The absolute bioavailability of Atorvastatin is approximately 14% and the systemic availability of HMG-CoA reductase inhibitory activity is approximately 30%. Mean volume of distribution is approximately 381 liters. Atorvastatin is ≥ 98% bound to plasma proteins. Atorvastatin is extensively metabolized to ortho-and para hydroxylated derivatives and various beta-oxidation products. Approximately 70% of circulatory inhibitory activity for HMG-CoA reductase is attributed to active metabolites. Atorvastatin and its metabolites are eliminated primarily in bile following hepatic and/or extrahepatic metabolism; however the drug does not appear to undergo enterohepatic recirculation. Mean plasma elimination half life of Atorvastatin in humans is approximately 14 hrs, but the half life of inhibitory activity for HMG-CoA reductase is 20-30 hours due to contribution of active metabolites.

Approx. Rs 120 / Pack(s) Get Latest Price

Mechanism of Action:

• Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Telmisartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland. Its action is therefore independent of the pathways for angiotensin II synthesis.
• There is also an AT2 receptor found in many tissues, but AT2 is not known to be associated with cardiovascular homeostasis. Telmisartan has much greater affinity (> 3,000 fold) for the AT1 receptor than for the AT2 receptor.
• Blockade of the renin-angiotensin system with ACE inhibitors, which inhibit the biosynthesis of angiotensin II from angiotensin I, is widely used in the treatment of hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Because telmisartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known. Telmisartan does not bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation.
• Blockade of the angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increased plasma renin activity and angiotensin II circulating levels do not overcome the effect of telmisartan on blood pressure.

Approx. Rs 83 / Pack Get Latest Price

Pharmacokinetics:

• Telmisartan is orally well absorbed and metabolized to an active metabolite which is more potent than Losartan as AT1 antagonist. Orally administered hydrochlorothiazide is rapidly absorbed and diuretic effect is seen in 1 hour and their duration lasts up to 12-24 hours. Both telmisartan and hydrochlorothiazide has longer duration of actions. These agents are bound to plasma proteins to varying degrees and this has no correlation to their half-life.

Approx. Rs 55 / Pack Get Latest Price

Mechanism of Action:

• Nicorandil, a vasodilator, is prescribed for the treatment and management of angina pectoris. The drug relaxes the blood vessels and alleviates the angina

Approx. Rs 25 / Pack Get Latest Price

Pharmacodynamics:

• Pharmacotherapeutic group: Quinolone antibacterials - Fluoroquinolones
• ATC code: J01MA12
• Levofloxacin is a synthetic antibacterial agent of the fluoroquinolone class and is the S(-) enatiomer of the racemic drug substance ofloxacin

Mechanism of Action:

• Levofloxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria. Like all quinolones, it functions by inhibiting the two type II topoisomerase enzymes, namely DNA gyrase and topoisomerase IV. Topoisomerase IV is necessary to separate DNA that has been replicated (doubled) prior to bacterial cell division. With the DNA not being separated, the process is stopped, and the bacterium cannot divide. DNA gyrase, on the other hand, is responsible for supercoiling the DNA, so that it will fit in the newly formed cells. Both mechanisms amount to killing the bacterium, that is, levofloxacin acts as a bactericide.

Pharmacokinetics

Absorption:

• Orally administered Levofloxacin is rapidly and almost completely absorbed with peak plasma concentrations being obtained within 1- 2 h. The absolute bioavailability is 99- 100 %
• Food has little effect on the absorption of Levofloxacin
• Steady state conditions are reached within 48 hours following a 500 mg once or twice daily dosage regimen. Distribution: Widely distributed in bronchial mucosa, lungs; CSF (relatively poor)
• Protein-Binding: 30-40%
• Metabolism: Levofloxacin is stereochemically stable in plasma and urine and does not invert metabolically to its enantiomer, D-ofloxacin. Levofloxacin undergoes limited metabolism in humans and is primarily excreted as unchanged drug in the urine.Following oral administration, approximately 87% of an administered dose was recovered as unchanged drug in urine within 48 hours, whereas less than 4% of the dose was recovered in feces in 72 hours. Less than 5% of an administered dose was recovered in the urine as the desmethyl and N-oxide metabolites, the only metabolites identified in humans. These metabolites have little relevant pharmacological activity.
• Excretion: Mainly via urine (largely as unchanged drug); 6-8 hours (elimination half-life)

Approx. Rs 65.41 / Strip Get Latest Price

We provide our precious clients the optimum quality range of Ucoliv 500mg Tablet. This tablet is used to treat bacterial infections of the skin, sinuses, kidneys, and bladder. Offered tablet is exclusively processed at our sound manufacturing unit using supreme class chemical compounds with the help of ultra-modern techniques under the guidance of diligent workforce. This tablet is widely acknowledged by our clients for its long shelf life and effectiveness.

Features:

• Safe consumption
• Accurate composition
• No side effects

Approx. Rs 395 / Pack Get Latest Price

Mechanism of Action:

• From above discussion we come to know that it is useful against cerebrovascular disease such as stroke, so it is necessary to know that how citicoline work in body. We know that the extensive damage caused by stroke requires repair and regeneration of axons and synapses of neurons, so new membrane production is essential. The primary mechanism by which citicoline is believed to have a therapeutic effect in stroke is its ability to increase the synthesis of phosphatidylcholine, the primary neuronal membrane component.
• It also enhances acetylcholine synthesis, and might thus ameliorate symptoms caused by the stroke induced los of cholinergic neurons. Another mechanism by which citicoline may have a more acute effect on the outcome of stroke patients relates to its ability to reduce free fatty acid accumulation at the site of injury, and thus to prevent further damage.
• Citicoline avoids, reduces of reverses the effects of ischemia and/or hypoxia in major part of animals and cellular models studied and acts in the cranial traumatic forms, reduces and limits the injuries to the membranes of the nerve cells, re – establishes the sensitivity and the functions of the regulatory intracellular enzymes and accelerates the re- absorption of the cerebral edema.
• Thus considerable evidence accumulated supports the use of citicoline for increasing and maintaining and repairing the membranes and the neuronal function in situations such as ischemia and traumatic injuries. In patients with senile dementia, citicoline reduces the evolution of damages.

Approx. Rs 39 / Pack(s) Get Latest Price

Pharmacotherapeutic group:

• Drugs used in diabetes; blood glucose lowering drugs, excl. insulins; ATC code: .
• Pioglitazone effects may be mediated by a reduction of insulin resistance. Pioglitazone appears to act via activation of specific nuclear receptors (peroxisome proliferator activated receptor gamma) leading to increased insulin sensitivity of liver, fat and skeletal muscle cells in animals. Treatment with pioglitazone has been shown to reduce hepatic glucose output and to increase peripheral glucose disposal in the case of insulin resistance.
• Fasting and postprandial glycaemic control is improved in patients with type 2 diabetes mellitus. The improved glycaemic control is associated with a reduction in both fasting and postprandial plasma insulin concentrations. A clinical trial of pioglitazone vs. gliclazide as monotherapy was extended to two years in order to assess time to treatment failure (defined as appearance of HbA1c ≥ 8.0 % after the first six months of therapy). Kaplan-Meier analysis showed shorter time to treatment failure in patients treated with gliclazide, compared with pioglitazone. At two years, glycaemic control (defined as HbA1c < 8.0 %) was sustained in 69 % of patients treated with pioglitazone, compared with 50 % of patients on gliclazide. In a two-year study of combination therapy comparing pioglitazone with gliclazide when added to metformin, glycaemic control measured as mean change from baseline in HbA1c was similar between treatment groups after one year. The rate of deterioration of HbA1c during the second year was less with pioglitazone than with gliclazide.

Approx. Rs 74 / Pack Get Latest Price

Mechanism of Action:

• Mechanism of action Alpha-glucosidase inhibitors are saccharides that act as competitive inhibitors of enzymes needed to digest carbohydrates: specifically alpha-glucosidase enzymes in the brush border of the small intestines. The membrane-bound intestinal alpha-glucosidases hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the small intestine. Acarbose also blocks pancreatic alpha-amylase in addition to inhibiting membrane-bound alpha-glucosidases. Pancreatic alpha-amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine. Inhibition of these enzyme systems reduces the rate of digestion of complex carbohydrates. Less glucose is absorbed because the carbohydrates are not broken down into glucose molecules. In diabetic patients, the short-term effect of these drugs therapies is to decrease current blood glucose levels: the long term effect is a small reduction in hemoglobin-A1c level.

Approx. Rs 45 / Pack Get Latest Price

Pharmacodynamics:

Amlodipine is a calcium ion influx inhibitor of the dihydropyridine group (calcium ion antagonist) and inhibits the transmembrane influx of calcium ions into cardiac and vascular smooth muscle. The mechanism of the antihypertensive action is due to a direct relaxant effect on vascular smooth muscle. Amlodipine reduces total ischaemic burden by the following actions:Amlodipine dilates peripheral arterioles and thus, reduces the total peripheral resistance (afterload) against which the heart works. Since the heart rate remains stable, this unloading of the heart reduces myocardial energy consumption and oxygen requirements.The mechanism of action of Amlodipine also probably involves dilatation of the main coronary arteries and coronary arterioles, both in normal and ischaemic regions. This dilation increases myocardial oxygen delivery in patients with coronary artery spasm.Atenolol is a beta-adrenoceptor blocking agent which is cardio-selective; its principal action is on beta-adrenergic receptors in the heart. It is without intrinsic sympathomimetic and membrane stabilising activities and as with other beta-blockers, has negative inotropic effects. It is probably assumed that the action of atenolol in reducing cardiac rate and contractility which makes it effective in eliminating or reducing the symptoms of patients with angina.

Approx. Rs 110 / Pack Get Latest Price

Mechanism of Action:

• Atorvastatin Calcium is a selective, competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3methylglutaryl-coenzyme A to mevalonate, a precursor of sterols, including cholesterol. Cholesterol and triglycerides circulate in the bloodstream as part of lipoprotein complexes. With ultracentrifugation, these complexes separate into HDL (high-density lipoprotein), IDL (intermediate-density lipoprotein), LDL (low-density lipoprotein), and VLDL (very-low-density lipoprotein) fractions. Triglycerides (TG) and cholesterol in the liver are incorporated into VLDL and released into the plasma for delivery to peripheral tissues. LDL is formed from VLDL and is catabolized primarily through the high-affinity LDL receptor. Clinical and pathologic studies show that elevated plasma levels of total cholesterol (total-C), LDL-cholesterol (LDL-C), and apolipoprotein B (apo B) promote human atherosclerosis and are risk factors for developing cardiovascular disease, while increased levels of HDL-C are associated with a decreased cardiovascular risk.
• In animal models, Atorvastatin Calcium lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the cell surface to enhance uptake and catabolism of LDL; Atorvastatin Calcium also reduces LDL production and the number of LDL particles. Atorvastatin Calcium reduces LDL-C in some patients with homozygous familial hypercholesterolemia (FH), a population that rarely responds to other lipid-lowering medication(s).
• A variety of clinical studies have demonstrated that elevated levels of total-C, LDL-C, and apo B (a membrane complex for LDL-C) promote human atherosclerosis. Similarly, decreased levels of HDL-C (and its transport complex, apo A) are associated with the development of atherosclerosis. Epidemiologic investigations have established that cardiovascular morbidity and mortality vary directly with the level of total-C and LDL-C, and inversely with the level of HDL-C.
• Atorvastatin Calcium reduces total-C, LDL-C, and apo B in patients with homozygous and heterozygous FH, nonfamilial forms of hypercholesterolemia, and mixed dyslipidemia. Atorvastatin Calcium also reduces VLDL-C and TG and produces variable increases in HDL-C and apolipoprotein A-1. Atorvastatin Calcium reduces total-C, LDL-C, VLDL-C, apo B, TG, and non-HDL-C, and increases HDL-C in patients with isolated hypertriglyceridemia. Atorvastatin Calcium reduces intermediate density lipoprotein cholesterol (IDL-C) in patients with dysbetalipoproteinemia.
• Like LDL, cholesterol-enriched triglyceride-rich lipoproteins, including VLDL, intermediate density lipoprotein (IDL), and remnants, can also promote atherosclerosis. Elevated plasma triglycerides are frequently found in a triad with low HDL-C levels and small LDL particles, as well as in association with non-lipid metabolic risk factors for coronary heart disease. As such, total plasma TG has not consistently been shown to be an independent risk factor for CHD. Furthermore, the independent effect of raising HDL or lowering TG on the risk of coronary and cardiovascular morbidity and mortality has not been determined.

Approx. Rs 48 / Pack Get Latest Price

Mechanism of Action:

• Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Telmisartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland. Its action is therefore independent of the pathways for angiotensin II synthesis.
• There is also an AT2 receptor found in many tissues, but AT2 is not known to be associated with cardiovascular homeostasis. Telmisartan has much greater affinity (> 3,000 fold) for the AT1 receptor than for the AT2 receptor.
• Blockade of the renin-angiotensin system with ACE inhibitors, which inhibit the biosynthesis of angiotensin II from angiotensin I, is widely used in the treatment of hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Because telmisartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known. Telmisartan does not bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation.
• Blockade of the angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increased plasma renin activity and angiotensin II circulating levels do not overcome the effect of telmisartan on blood pressure.

Approx. Rs 168 / Pack(s) Get Latest Price

We are a well-renowned organization in the industry to provide our patrons the best quality array of Atmofix Oz Tablets. Under the stern guidance of deft workforce, the offered tablet is well-processed using optimum class chemical compounds and sophisticated technology in tandem with the set medical industry norms. Moreover, this tablet is precisely tested against several parameters of quality to avoid any kind of impurity. The provided tablet is used to treat a wide variety of bacterial infections.

Features:

• Free from side effects
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Approx. Rs 120 / Strip Get Latest Price

composition :- Gabapentin 300 mg, Mecobalamin 500 mcg

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