CAPTOPRIL tablet

国: アメリカ合衆国

言語: 英語

ソース: NLM (National Library of Medicine)

有効成分:

CAPTOPRIL (UNII: 9G64RSX1XD) (CAPTOPRIL - UNII:9G64RSX1XD)

から入手可能:

Avera McKennan Hospital

INN（国際名）:

CAPTOPRIL

構図:

CAPTOPRIL 50 mg

処方タイプ:

PRESCRIPTION DRUG

認証ステータス:

Abbreviated New Drug Application

製品の特徴

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