Hydrochlorothiazide

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Hydrochlorothiazide
Systematic (IUPAC) name
6-chloro-3,4-dihydro-2H-
1,2,4-benzothiadiazine-
7-sulfonamide 1,1-dioxide
Identifiers
CAS number 58-93-5
ATC code C03AA03
PubChem 3639
Chemical data
Formula C7H8ClN3O4S2 
Mol. mass 297.742
SMILES eMolecules & PubChem
Pharmacokinetic data
Bioavailability Variably absorbed from GI tract
Metabolism does not undergo significant metabolism (>95% excreted unchanged in urine)[1]
Half life 5.6-14.8 hours
Excretion Primarily excreted unchanged in urine
Therapeutic considerations
Pregnancy cat.

B (D if used to treat pregnancy-induced hypertension)

Legal status

Prescription only

Routes Oral (capsules, tablets, oral solution)

Hydrochlorothiazide, sometimes abbreviated HCT, HCTZ, or HZT is a popular diuretic drug of the thiazide class that acts by inhibiting the kidneys' ability to retain water. This reduces the volume of the blood, decreasing blood return to the heart and thus cardiac output and, by other mechanisms, is believed to lower peripheral vascular resistance. Hydrochlorothiazide is sold both as a generic drug and under a large number of brand names, including: Apo-Hydro, Aquazide H, Dichlotride, Hydrodiuril, HydroSaluric, Microzide, Oretic.

Contents

Activity

Hydrochlorothiazide belongs to the thiazide class of diuretics, acting on the kidneys to reduce sodium (Na) reabsorption in the distal convoluted tubule. This increases the osmolarity in the lumen, causing less water to be reabsorbed by the collecting ducts. This leads to increased urinary output.

Indications

HCT is often used in the treatment of hypertension, congestive heart failure, symptomatic edema and the prevention of kidney stones. It is effective for nephrogenic diabetes insipidus (paradoxical effect, which decreases urine formation) and is also sometimes used for hypercalciuria and Dent's Disease.

Hypokalemia, an occasional side-effect, can be usually prevented by potassium supplements or combining hydrochlorothiazide with a potassium-sparing diuretic.

Thiazides are also used in the treatment of osteoporosis. Thiazides decrease mineral bone loss by promoting calcium retention in the kidney, and by directly stimulating osteoblast differentiation and bone mineral formation.[2]

Side effects

External links


References

  1. ^ Beermann B, Groschinsky-Grind M, Rosén A. (1976). "Absorption, metabolism, and excretion of hydrochlorothiazide". Clin Pharmacol Ther 19 (5 (Pt 1)): 531–7. 
  2. ^ Dvorak MM, De Joussineau C, Carter DH, et al (2007). "Thiazide diuretics directly induce osteoblast differentiation and mineralized nodule formation by interacting with a sodium chloride co-transporter in bone". J. Am. Soc. Nephrol. 18 (9): 2509–16. doi:10.1681/ASN.2007030348. PMID 17656470. 


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  • This page was last modified on 1 July 2008, at 13:44.

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