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Thiazide diuretics have been the 'mainstay' of antihypertensive therapy for three decades. They reduce arterial pressure, initially through a fall in plasma volume and cardiac output. However, in time, output returns towards pretreatment levels, thereby accounting for a long-term fall in pressure through decreased vascular resistance. At present, the precise mechanism for this reduced resistance remains unknown. Although the fall in arterial pressure is not due to direct vasodilation, it is not unlikely that it may operate, in part, indirectly through reduced vascular responsiveness, induced prostacyclins and other mechanisms. Attendant unwanted biochemical effects include hypokalaemia, hyperuricaemia, hyperglycaemia, reduced renal excretory function and hyperlipidaemia. Orthostatic hypotension and, of more recent emphasis, sexual impotence are among the more common side effects. A question has been raised as to whether hyperlipidaemia might explain the failure of some multicentre studies to prevent myocardial infarction or progression of coronary heart disease but this is more a 'non issue' although it must be considered. The present data continue to support the conclusion that diuretics are safe, effective and economical for the treatment of hypertension, and they remain a major cornerstone of initial as well as multipharmacological therapy, particularly in volume-dependent forms of essential hypertension, steroid-dependent hypertensions, renal parenchymal disease and in special patient groups (black, obese and elderly).