CAPTOPRIL-100 TAB 100MG TABLET

Country: Kanada

Lingwa: Ingliż

Sors: Health Canada

Ingredjent attiv:

CAPTOPRIL

Disponibbli minn:

PRO DOC LIMITEE

Kodiċi ATC:

C09AA01

INN (Isem Internazzjonali):

CAPTOPRIL

Dożaġġ:

100MG

Għamla farmaċewtika:

TABLET

Kompożizzjoni:

CAPTOPRIL 100MG

Rotta amministrattiva:

ORAL

Unitajiet fil-pakkett:

100/500/1000

Tip ta 'preskrizzjoni:

Prescription

Żona terapewtika:

ANGIOTENSIN-CONVERTING ENZYME INHIBITORS

Sommarju tal-prodott:

Active ingredient group (AIG) number: 0114954003; AHFS:

L-istatus ta 'awtorizzazzjoni:

CANCELLED POST MARKET

Data ta 'l-awtorizzazzjoni:

2000-07-31

Karatteristiċi tal-prodott

0
PRODUCT MONOGRAPH
PR
CAPTOPRIL
CAPTOPRIL TABLETS USP
12.5, 25, 50 AND 100 MG
ANGIOTENSIN-CONVERTING ENZYME INHIBITOR
PRO DOC LTÉE
DATE OF REVISION:
2925, BOUL. INDUSTRIEL
March 7, 2008
LAVAL, QUÉBEC
H7L 3W9
Control number : 111881
1
PRODUCT MONOGRAPH
Pr
CAPTOPRIL
Captopril Tablets USP
12.5, 25, 50 and 100 mg
THERAPEUTIC CLASSIFICATION
Angiotensin-Converting Enzyme Inhibitor
ACTIONS AND CLINICAL PHARMACOLOGY
Captopril is an angiotensin converting enzyme inhibitor which is used
in the treatment of
hypertension and heart failure.
The mechanism of action of captopril has not yet been fully
elucidated. It appears to lower blood
pressure and be an adjunct in the therapy of congestive heart failure
primarily through
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.
Captopril prevents the conversion of angiotensin I to angiotensin II
by inhibition of ACE, a
peptidyldipeptide carboxy hydrolase.
ACE is identical to ‘bradykininase’, and captopril may also
interfere with the degradation of the
vasodepressor peptide, bradykinin. However, the effectiveness of
captopril in therapeutic doses
appears to be unrelated to potentiation of the actions of bradykinin.
Increased concentrations of
bradykinin or prostaglandin E
2
may also have a role in the therapeutic effect of captopril,
especially in low-renin hypertension.
Inhibition of ACE results in decreased plasma angiotensin II and
increased plasma renin activity
(PRA), the latter resulting from loss of negative feedback on renin
rel