What is the mechanism of action of hydrochlorothiazide regarding urine output?

Hydrochlorothiazide is a thiazide diuretic, and its primary mechanism of action involves increasing the excretion of sodium. It works on the distal convoluted tubule of the kidney, where it inhibits the sodium-chloride symporter. By blocking this transporter, hydrochlorothiazide prevents the reabsorption of sodium back into the bloodstream. As a result, sodium remains in the tubular fluid, leading to an increase in osmotic pressure that draws water along with it into the urine. This process ultimately increases urine output.

Additionally, with sodium being excreted, there is also an increase in the excretion of water, leading to diuresis. As a consequence of the loss of sodium and water, blood volume decreases, which can help in the management of hypertension and edema.

Other options do not accurately represent the key actions of hydrochlorothiazide. While the drug does affect fluid dynamics in the kidneys, its primary contribution to increased urine output is through the excretion of sodium rather than reabsorption of potassium, direct alteration of glomerular filtration rate, or inhibition of neurotransmitters.