NTP-CLONIDINE TABLET

Valsts: Kanāda

Valoda: angļu

Klimata pārmaiņas: Health Canada

Aktīvā sastāvdaļa:

CLONIDINE HYDROCHLORIDE

Pieejams no:

TEVA CANADA LIMITED

ATĶ kods:

C02AC01

SNN (starptautisko nepatentēto nosaukumu):

CLONIDINE

Deva:

0.2MG

Zāļu forma:

TABLET

Kompozīcija:

CLONIDINE HYDROCHLORIDE 0.2MG

Ievadīšanas:

ORAL

Vienības iepakojumā:

100/500

Receptes veids:

Prescription

Ārstniecības joma:

CENTRAL ALPHA-AGONISTS

Produktu pārskats:

Active ingredient group (AIG) number: 0108891002; AHFS:

Autorizācija statuss:

CANCELLED PRE MARKET

Autorizācija datums:

2015-08-06

Produkta apraksts

PRODUCT MONOGRAPH
Pr
NTP-CLONIDINE
(Clonidine Hydrochloride)
0.1 and 0.2 mg Tablets
USP
Antihypertensive
Teva Canada Ltd.
30 Novopharm Court
Toronto, Ontario
Canada, M1B 2K9
Submission Control No: 165993
Date of Preparation:
July 17, 2013
PRODUCT MONOGRAPH
NTP-CLONIDINE
(Clonidine Hydrochloride)
0.1 and 0.2 mg Tablets
USP
THERAPEUTIC CLASSIFICATION
Antihypertensive Agent
ACTION AND CLINICAL PHARMACOLOGY
Clinically, the principal effects seen with NTP-CLONIDINE (clonidine
hydrochloride) are
consistent with a direct action of the drug on the vasomotor centres
in the brain stem. There is no
blockade of peripheral ganglia, neurons or receptors. In animals,
following clonidine
administration, spontaneous sympathetic discharges from the medullary
centres are reduced. A
lowered tone of the vasomotor centres rather than blockade is
suggested by the differential action
on spontaneous and evoked central sympathetic impulses. Thus,
clonidine has the ability to
lower blood pressure while preserving normal homeostatic mechanisms.
A pressor phase is not seen if the drug is given intramuscularly or
orally, although with
intravenous use of the drug a transient rise in blood pressure may
precede the prolonged period
of hypotension. The pressor phase following intravenous clonidine has
been shown to be due to a
direct effect of the drug on peripheral α-receptors, and this phase
of the blood pressure effect and
the depressor phase can be reversed by α-blocking drugs. It has been
suggested therefore, that
clonidine exerts an action on postulated central α-receptors in a
manner similar to the action in
the periphery. The prolonged hypotensive phase may thus result from
two opposing actions each
mediated by α-receptors.
Effects on Catecholamines, Renin and Aldosterone:
Tissue stores of catecholamines are not depleted by clonidine.
However, as would be expected
with central depression of sympathomimetic activity, clonidine therapy
results in diminished
urinary excretion of catecholamines. Conversely, there may be a sharp
increase i