The thiazides act in the distal tubule to decrease sodium reabsorption (inhibits Na/Cl transporter). As a result of decreased sodium and chloride reabsorption, a hyperosmolar diuresis ensues.

Delivery of more sodium to the distal tubule results in potassium loss by an exchange mechanism.

Thiazides also promote calcium reabsorption, in contrast to loop diuretics.

The initial decrease in blood volume followed by a longer-termed reduction in vascular resistance appears to account for the hypotensive effects of the thiazides.

Adverse Effects-

• Potassium depletion is a potentially serious side-effect that may require potassium supplementation and/or concurrent use of potassium-sparing diuretics.

• Hyperuricemia may occur precipitating gout. The increase in systemic uric acid is due to a decrease in the effectiveness of the organic acid secretory system

• Diabetic patient may have difficulty in maintaining proper blood sugar levels.