Drug breakdown: Indapamide
Abstract
In this column, Sharon Rees aims to refresh knowledge and interest in some of the commonly used drugs in a series of tweets. This month she is talking about #Indapamide
Dr Sharon Rees @reesprescribe
Day 1: Labelled a ‘thiazide-like’ diuretic (as it acts in the distal convoluted tubule), #indapamide is actually a non-thiazide sulfonamide. Derived in the late 1960s from benzamide (found in plants eg autumn crocus), it was designed to retain blood pressure lowering effect, as distinct from diuresis.
Dr Sharon Rees @reesprescribe
Day 2: Oral formation only for #indapamide. In the UK, licensed use for essential hypertension at 2.5 mg once daily, or modified release 1.5 mg once daily.
Dr Sharon Rees @reesprescribe
Day 3: Kinetics #indapamide; good oral absorption, cmax 1–2 hours. Binds to red blood cells and plasma proteins, and is then taken up through vascular walls where it acts. Liver metabolism via CYP3A4 with one active metabolite. Renal excretion (avoid in severe impairment), but ~ 23% gastrointestinal excretion. T½ 15–18 hours.
Dr Sharon Rees @reesprescribe
Day 4: MOA; #indapamide lowers blood pressure mainly via vascular action (as opposed to diuresis) by reducing calcium uptake in vascular smooth muscle, leading to impaired vasoconstriction. Also more vasodilation via increased prostaglandin levels (PGE2 and prostacyclin) and increased bradykinin levels (also all relevant to reduced platelet aggregation). #indapamide also reduces left ventricular hypertrophy.
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