A1,
A2,
B,
C1,
C2,
D,
E,
F,
G-H,
I-K,
L,
M,
N,
O,
P1,
P2,
Q-R,
S,
T,
U-V,
W-Z
Catapres-TTS Pharmacology, Pharmacokinetics, Studies, Metabolism - Clonidine Patch
Catapres-TTS Pharmacology, Pharmacokinetics, Studies, Metabolism - Clonidine Patch
CLINICAL PHARMACOLOGY
Clonidine stimulates alpha-adrenoreceptors in the brain
stem, resulting in reduced sympathetic
outflow from the central
nervous system
and a decrease in peripheral
resistance, renal vascular
resistance, heart rate,
and blood pressure. Renal blood
wflow and glomerular
filtration rate
remain essentially unchanged. Normal postural
reflexes are intact, and therefore orthostatic symptoms are mild
and infrequent.
Acute studies with clonidine hydrochloride
in human have demonstrated
a moderate reduction
(15% to 20%) of cardiac
output in the supine
position with no change in the peripheral
resistance; at a 45° tilt there is a smaller reduction
in cardiac output
and a decrease of peripheral
resistance. During long-term therapy, cardiac
output tends to return
to control values, while
peripheral resistance
remains decreased. Slowing of the pulse
rate has been observed
in most patients given clonidine, but the drug
does not alter normal hemodynamic response
to exercise.
Other studies in patients have provided evidence
of a reduction in
plasma renin activity and in the excretion
of aldosterone and
catecholamines, but the exact relationship of these pharmacologic
actions to the antihypertensive effect has not been fully elucidated.
Clonidine acutely stimulates growth
hormone release
in both children and adults, but does not produce a chronic
elevation of growth
hormone with long-term
use.
Tolerance may develop in some patients, necessitating a reevaluation
of therapy.
The plasma half-life
of clonidine is 12.7 ±7 hours. Following
oral administration
about 40-60% of the absorbed dose
is recovered in the urine as unchanged drug
in 24 hours. About 50% of the absorbed dose
is metabolized in the liver.
top
