A thiazide is any of a group of diuretics that act by inhibiting the reabsorption of sodium and chloride in the in the distal renal tubule. This action results in increased sodium and free water clearance. A secondary effect is the loss of potassium by increased secretion in the distal tubule (in response to increased intraluminal sodium concentration).
The reduction in plasma and extracellular fluid volume leads to the activation of a counter-regulatory system mediated by renin-angiotensin-aldosterone and adrenergic systems in an attempt to re-establish central blood volume. This activation of the counter-regulatory system may last up to nine days and is an explanation for the variable interpersonal antihypertensive efficacy (1).
They are used in the treatment of hypertension and of heart failure.
The ALLHAT data revealed that diuretics were superior to calcium channel blockers and, at least in the short term, angiotensin-converting enzyme inhibitors in preventing heart failure in hypertensive individuals.
Thiazides, like all diuretics (other than K+ sparing), exert their effect based on intraluminal, rather than serum drug concentrations (3)
Measure serum electrolytes and creatinine one to two weeks after initiation of a thiazide, whether it is being used for hypertension or for heart failure (3)
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