What is the mechanism of action for hydrochlorothiazide as it affects the kidneys?

Hydrochlorothiazide primarily functions as a thiazide diuretic, and its mechanism of action involves blocking the sodium-chloride transporter located in the distal convoluted tubule of the nephron in the kidneys. By inhibiting this transporter, hydrochlorothiazide prevents the reabsorption of sodium and chloride ions back into the bloodstream. As a result, more sodium and chloride remain in the renal tubule, leading to increased osmotic pressure, which causes water to be excreted along with these electrolytes. This diuretic effect helps reduce blood volume and, consequently, lower blood pressure, making hydrochlorothiazide effective in managing hypertension and conditions associated with fluid retention.

The other options do not accurately describe the primary action of hydrochlorothiazide. For example, increasing sodium reabsorption contradicts its function, as it aims to reduce sodium retention and promote its excretion. Similarly, increasing water retention would be the opposite effect of what thiazide diuretics aim to achieve, and inhibiting aldosterone secretion is not a direct mechanism of hydrochlorothiazide; rather, it primarily acts on the sodium-chloride transporter.