Co-Amlessa

Indapamide is a diuretic agent.‍‍‍‍‍‍​​​‍​​​​​​ It inhibits sodium reabsorption in the cortical renal tubules, thereby increasing urinary excretion of sodium and chloride ions and consequently increasing urine output. However, its blood pressure-lowering effect is attributable to a different mechanism. Indapamide gradually reduces blood pressure through its effect on blood vessels — it decreases peripheral vascular resistance. Indapamide reduces peripheral resistance by: decreasing vascular smooth muscle contractility (primarily through effects on calcium transport); dilating blood vessels (through stimulation of prostaglandin PGE2 and prostacyclin PGI2 production, and potentiation of bradykinin action); reducing vascular sensitivity to adrenaline. Indapamide also reduces left ventricular hypertrophy. Indapamide is absorbed rapidly and almost completely from the gastrointestinal tract. The presence of food slightly affects the rate of absorption but does not affect the amount of drug absorbed. Peak plasma concentration is reached approximately 12 hours after administration. Indapamide is 79% bound to plasma proteins. The elimination half-life is approximately 18 hours (range 14 to 24 hours). Repeated administration does not lead to accumulation. Steady state is achieved after approximately 7 days. Indapamide is primarily metabolised in the liver to inactive metabolites. Approximately 90% of the drug is excreted as inactive metabolites: 70% renally in the urine and 20% in the faeces.