m-Captopril

Country: New Zealand

Language: English

Source: Medsafe (Medicines Safety Authority)

Active ingredient:

Captopril 50mg;  

Available from:

Multichem NZ Limited

INN (International Name):

Captopril 50 mg

Dosage:

50 mg

Pharmaceutical form:

Tablet

Composition:

Active: Captopril 50mg   Excipient: Colloidal silicon dioxide Lactose Maize starch Microcrystalline cellulose Palmitic acid Purified talc

Units in package:

Bottle, plastic, HDPE; polypropylene cap (100), 100 tablets

Class:

Prescription

Prescription type:

Prescription

Manufactured by:

Wockhardt Ltd

Product summary:

Package - Contents - Shelf Life: Bottle, plastic, HDPE; polypropylene cap (100) - 100 tablets - 36 months from date of manufacture stored at or below 25°C protect from light and moisture - Bottle, plastic, HDPE; polypropylene cap (500) - 500 tablets - 36 months from date of manufacture stored at or below 25°C protect from light and moisture - Bottle, plastic, HDPE; polypropylene cap (1000) - 1000 tablets - 36 months from date of manufacture stored at or below 25°C protect from light and moisture

Authorization date:

2003-10-23

Summary of Product characteristics

NEW ZEALAND DATA SHEET 
M-CAPTOPRIL 
Captopril 12.5mg, 25mg, 50mg and 100mg tablet USP 

PRESENTATION  
m-Captopril 12.5mg tablets are white to off-white, round flat tablets
with beveled 
edges with W over 902 debossed on one surface and break line on the
other.  
m-Captopril 25mg tablets are white to off-white, round flat tablets
with beveled edges 
with W over 903 debossed on one surface and cross line on the other.

m-Captopril 50mg tablets are white to off-white, round flat tablets
with beveled edges 
with W over 904 debossed on one surface and break line on the other.

m-Captopril 100mg tablets are white to off-white, round flat tablets
with beveled 
edges with W over 905 debossed on one surface and break line on the
other.  

USES  
ACTIONS  
Captopril is a sulfhydryl-containing angiotensin-converting enzyme
(ACE) inhibitor 
used in the treatment of hypertension and heart failure.  
Although its exact mode of action is not fully elucidated, most of
the beneficial effects 
appear to result from suppression of the
renin-angiotensin-aldosterone system. 
However since it also effectively reduces blood pressure in
patients with low renin 
concentrations other mechanisms are probably also involved.  
The formation of angiotensin I is mediated by renin, an enzyme
released into the 
circulation by the kidneys in response to a low circulating blood
volume or blood 
pressure.  
Captopril prevents the conversion of angiotensin I, to angiotensin II
by competing for 
the angiotensin-converting enzyme (ACE). Reduction of angiotension II
results in 
decreased aldosterone secretion which results in sodium and fluid
loss together with 
small increases in serum potassium. Additional effects of captopril
on bradykinin and 
prostaglandins are also postulated.  
The hypotensive effect of captopril persists for a longer of
time than inhibition of ACE 
in the blood. It is not known whether ACE present in
vascular endothelium is inhibited 
longer