Mechanisms of Action
The members of this class of diuretics are derived from benzothiadiazine. They control hypertension in part by inhibiting reabsorption of sodium (Na+) and chloride (Cl−) ions from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl− symporter. The term "thiazide" is also often used for drugs with a similar action that do not have the thiazide chemical structure, such as chlortalidone and metolazone. These agents are more properly termed thiazide-like diuretics.
Thiazide diuretics also increase calcium reabsorption at the distal tubule. By lowering the sodium concentration within the epithelial cells, thiazides increase the activity of the Na+/Ca2+-ATPase on the basolateral membrane to pump more Ca2+ into the interstitium. This, in turn, lowers the intracellular Ca2+ concentration so that more Ca2+ may diffuse into the cell via apical Ca2+-selective channels (TRPV5) --> (In other words, less Ca++ in the cell creates a force for reabsorption from the lumen).
Thiazides are also thought to increase the reabsorption of Ca2+ by a mechanism involving the reabsorption of sodium and calcium in the proximal tubule in response to sodium depletion. Some of this response is due to augmentation of the action of parathyroid hormone.
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