Essential hypertension, hypertension in patients with renal function impairment, salt & fluid retention associated with congestive heart failure.
Indole derivative; Diuretic
Indapamide is an oral antihypertensive agent. The mechanism whereby Indapamide exerts its antihypertensive action has not been completely elucidated; both vascular and renal actions have been implicated. The possible beneficial pharmacological effects of Indapamide in the treatment of hypertension include a reduction in cardiac hypertrophy and a reduction in the thickening of arterial walls, a prevention of the accumulation of the embryonic isoform of fibronectin in coronary vessels, free radical scavenging leading to stimulation of vasodilator eicosanoid formation, and interaction with renal carbonic anhydrase. The renal site of action of Indapamide is the proximal segment of the distal tubule. Indapamide appears to have natriuretic properties (sodium and chloride being excreted in equivalent amounts) with less effect on kaliuresis or uric acid excretion. Only at doses greater than 1.5 mg Indapamide sustained release tablet/day is an appreciable increase in urinary volume observed in man. No significant changes in plasma sodium levels have been observed in clinical studies. Significant hypokalemia (plasma potassium <3.2 mmol/L) has been reported in 4% of patients.
Absorption: The fraction of Indapamide released is rapidly and totally absorbed via the gastrointestinal digestive tract. Ingestion with food slightly increases the rate and extent of absorption. These changes are unlikely to be clinically significant. Peak serum level following a single dose occurs about 12 hours after ingestion; repeated administration reduces the variation in serum levels between 2 doses.
Distribution: Indapamide is widely distributed throughout the body, with extensive binding to some specific sites. In blood, it is highly bound to red blood cells (80%) and more specifically to carbonic anhydrase (98%) without having any significant inhibiting activity on this enzyme. Binding of Indapamide to plasma proteins is 79%. The plasma elimination half-life is 14 to 24 hours (mean 18 hours). The drug has a volume of distribution of approximately 60L. Steady state is achieved after 7 days. Repeated administration does not lead to accumulation.
Metabolism: The drug is extensively metabolized in the liver, with only 5 to 7% of the dose excreted in the urine as unchanged drug.
Elimination: Elimination is essentially urinary (70% of the dose) and faecal (22%) in the form of inactive metabolites.
One tablet daily, preferably in the morning.
Other Antihypertensive: Indapamide may add to or potentiate the action of other antihypertensive drugs. In limited controlled trials that compared the effect of Indapamide combined with other antihypertensive drugs with the effect of the other drugs administered alone, there was no notable change in the nature or frequency of adverse reactions associated with the combined therapy.
Norepinephrine: Indapamide, like the thiazides, may decrease arterial responsiveness to norepinephrine, but this diminution is not sufficient to preclude effectiveness of the pressor agent for therapeutic use.
Known allergy to this drug or to sulphonamides, Renal failure, Serious liver disease, Hypokalemia, Disturbed water/electrolyte balance, diabetes, gout & kidney problems. Monitoring of Potassium & Uric acid serum levels is recommended.
Dizziness, headache, anorexia, nausea, vomiting, constipation, diarrhea & postural hypotension. Electrolyte imbalances include hypochloremic alkalosis, hyponatremia, hypokalemia, hyperuricemia; hypersensitivity reactions which include skin rashes, cholestatic jaundice & blood dyscrasias including thrombocytopenia, leucopenia, aplastic anemia.
In pregnant women Indapamide is not recommended. Mothers taking Indapamide should not breast feed.
Store in a cool and dry place. Protect from light and moisture.
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