Riik: Ameerika Ühendriigid
keel: inglise
Allikas: NLM (National Library of Medicine)
CAPTOPRIL (UNII: 9G64RSX1XD) (CAPTOPRIL - UNII:9G64RSX1XD)
Avera McKennan Hospital
CAPTOPRIL
CAPTOPRIL 50 mg
PRESCRIPTION DRUG
Abbreviated New Drug Application
CAPTOPRIL- CAPTOPRIL TABLET AVERA MCKENNAN HOSPITAL ---------- CAPTOPRIL TABLETS CAPTOPRIL TABLETS, USP Rev. 03/16 Rx Only WARNING: FETAL TOXICITY • WHEN PREGNANCY IS DETECTED, DISCONTINUE CAPTOPRIL TABLETS AS SOON AS POSSIBLE. • DRUGS THAT ACT DIRECTLY ON THE RENIN-ANGIOTENSIN SYSTEM CAN CAUSE INJURY AND DEATH TO THE DEVELOPING FETUS. SEE WARNINGS: FETAL TOXICITY DESCRIPTION Captopril Tablets, USP are a specific competitive inhibitor of angiotensin I-converting enzyme (ACE), the enzyme responsible for the conversion of angiotensin I to angiotensin II. Captopril is designated chemically as 1-[(2S)-3-mercapto-2-methylpropionyl]-L-proline and has the following structural formula: Captopril is a white to off-white crystalline powder that may have a slight sulfurous odor; it is soluble in water (approx. 160 mg/mL), methanol, and ethanol and sparingly soluble in chloroform and ethyl acetate. Each tablet for oral administration contains 12.5 mg, 25 mg, 50 mg or 100 mg of captopril. In addition, each tablet contains the following inactive ingredients: anhydrous lactose, colloidal silicon dioxide, microcrystalline cellulose, sodium starch glycolate (derived from potato), starch (derived from corn), and stearic acid. CLINICAL PHARMACOLOGY MECHANISM OF ACTION: The mechanism of action of captopril tablets has not yet been fully elucidated. Its beneficial effects in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin- aldosterone system. However, there is no consistent correlation between renin levels and response to the drug. Renin, an enzyme synthesized by the kidneys, is released into the circulation where it acts on a plasma globulin substrate to produce angiotensin I, a relatively inactive decapeptide. Angiotensin I is then converted by angiotensin converting enzyme (ACE) to angiotensin II, a potent endogenous vasoconstrictor substance. Angiotensin II also stimulates aldosterone secretion from the adrenal cortex, thereby contributing to sodium and fluid retention. Capt Lugege kogu dokumenti