Diuretic/Antihypertensive.
Pharmacology: Pharmacodynamics: Thiazide diuretics increase the excretion of water by inhibiting the reabsorption of sodium and chloride ions at the distal renal tubule. The natriuretic effects are accompanied by a secondary loss of potassium and bicarbonate which can cause a mild hypokalemic, hypochloremic, metabolic alkalosis. Thiazides also decrease the elimination of calcium and uric acid. Thiazide diuretics usually do not affect normal blood pressure. When chronically administered, thiazide diuretics decrease peripheral vascular resistance. The exact mechanism responsible for lowered peripheral resistance is not known. However, excretion of urinary sodium by the kidneys is required to achieve blood pressure reduction.
Pharmacokinetics: Hydrochlorothiazide (HCTZ) is absorbed from the GIT. HCTZ crosses the placental but not the blood-brain barrier and is distributed into breast milk. Based on determination of plasma-drug concentrations over a period of at least 24 hrs, the plasma t½ of HCTZ reportedly ranges from 5.6-14.8 hrs.
HCTZ is apparently metabolized and excreted unchanged in urine. At least 61% of the drug is reportedly eliminated from the body within 24 hrs.