Document
DailyMed Label: Benazepril Hydrochloride
Title
DailyMed Label: BENAZEPRIL
Date
2010
Document type
DailyMed Prescription
Name
BENAZEPRIL
Generic name
BENAZEPRIL HYDROCHLORIDE
Manufacturer
STAT RX USA LLC
Product information
NDC: 16590-259
Product information
NDC: 16590-259
Description
DESCRIPTION
Benazepril hydrochloride is a white to off-white crystalline
powder, soluble (>100 mg/mL) in water, in ethanol, and in methanol. Its
chemical name is
3-[[1-(ethoxy-carbonyl)-3-phenyl-(1S)-propyl]amino]-2,3,4,5-tetrahydro-2-oxo-1H-1-(3S)-benzazepine-1-acetic
acid monohydrochloride; its structural formula is
BENAZEPRIL 20MG STRUCTURE
Its empirical formula is C 24 H 28 N 2 O 5 •HCl, and
its molecular weight is 460.96.
Benazeprilat, the active metabolite of benazepril, is a non-sulfhydryl
angiotensin-converting enzyme inhibitor. Benazepril is converted to benazeprilat
by hepatic cleavage of the ester group.
Benazepril Hydrochloride Tablets, USP are supplied as white and round
biconvex tablets containing 5 mg, 10 mg, 20 mg, and 40 mg of benazepril
hydrochloride for oral administration. The inactive ingredients are
crospovidone, lactose anhydrous, magnesium stearate, microcrystalline cellulose,
pregelatinized corn starch, and talc.
BENAZEPRIL 20MG STRUCTURE
Indications
Benazepril hydrochloride is indicated for the treatment of
hypertension. It may be used alone or in combination with thiazide
diuretics.
In using Benazepril hydrochloride, consideration should be given to the fact
that another angiotensin-converting enzyme inhibitor, captopril, has caused
agranulocytosis, particularly in patients with renal impairment or
collagen-vascular disease. Available data are insufficient to show that
Benazepril hydrochloride does not have a similar risk (see WARNINGS ).
Black patients receiving ACE-inhibitors have been reported to have a higher
incidence of angioedema compared to nonblacks. It should also be noted that in
controlled clinical trials ACE inhibitors have an effect on blood pressure that
is less in black patients than in nonblacks
Dosage
Hypertension
Adults
The recommended initial dose for patients not receiving a diuretic is 10 mg
once-a-day. The usual maintenance dosage range is 20-40 mg per day administered
as a single dose or in two equally divided doses. A dose of 80 mg gives an
increased response, but experience with this dose is limited. The divided
regimen was more effective in controlling trough (pre-dosing) blood pressure
than the same dose given as a once-daily regimen. Dosage adjustment should be
based on measurement of peak (2-6 hours after dosing) and trough responses. If a
once-daily regimen does not give adequate trough response, an increase in dosage
or divided administration should be considered. If blood pressure is not
controlled with Benazepril hydrochloride alone, a diuretic can be added.
Total daily doses above 80 mg have not been evaluated.
Concomitant administration of Benazepril hydrochloride with potassium
supplements, potassium salt substitutes, or potassium-sparing diuretics can lead
to increases of serum potassium (see PRECAUTIONS ).
In patients who are currently being treated with a diuretic, symptomatic
hypotension occasionally can occur following the initial dose of Benazepril
hydrochloride. To reduce the likelihood of hypotension, the diuretic should, if
possible, be discontinued two to three days prior to beginning therapy with
Benazepril hydrochloride (see WARNINGS ). Then, if blood
pressure is not controlled with Benazepril hydrochloride alone, diuretic therapy
should be resumed.
If the diuretic cannot be discontinued, an initial dose of 5 mg benazepril
hydrochloride should be used to avoid excessive hypotension.
Pediatrics
In children, doses of Benazepril hydrochloride between 0.1 and 0.6 mg/kg once
daily have been studied, and doses greater than 0.1 mg/kg were shown to reduce
blood pressure (see Pharmacodynamics ). Based on
this, the recommended starting dose of Benazepril hydrochloride in 0.2 mg/kg
once per day as monotherapy. Doses above 0.6 mg/kg (or in excess of 40 mg daily)
have not been studied in pediatric patients.
For pediatric patients who cannot swallow tablets, or for whom the calculated
dosage (mg/kg) does not correspond to the available tablet strengths for
benazepril hydrochloride, follow the suspension preparation instructions below
to administer benazepril HCl as a suspension.
Treatment with benazepril hydrochloride is not advised for children below the
age of 6 years (see PRECAUTIONS, Pediatric Use ) and
in pediatric patients with glomerular filtration rate less than 30 mL, as there are
insufficient data available to support a dosing recommendation in these
groups.
For Hypertensive Patients with Renal Impairment
For patients with a creatinine clearance less than 30 mL/min/1.73 m 2 (serum creatinine greater than 3 mg/dL), the recommended initial dose
is 5 mg Benazepril hydrochloride once daily. Dosage may be titrated upward until
blood pressure is controlled or to a maximum total daily dose of 40 mg (see WARNINGS ).
Preparation of Suspension (for 150 mL of a 2 mg/mL
suspension)
Add 75 mL of Ora-Plus®*oral suspending vehicle to an amber polyethylene
terephthalate (PET) bottle containing fifteen Benazepril hydrochloride 20 mg
tablets, and shake for at least 2 minutes. Allow the suspension to stand for a
minimum of 1 hour. After the standing time, shake the suspension for a minimum
of 1 additional minute. Add 75 mL of Ora-Sweet®*oral syrup vehicle to the bottle
and shake the suspension to disperse the ingredients. The suspension should be
refrigerated at 2-8°C (36-46°F) and can be stored for up to 30 days in the PET
bottle with a child-resistant screw-cap closure. Shake the suspension before
each use.
*Ora-Plus® and Ora-Sweet® are registered trademarks of Paddock Laboratories,
Inc. Ora-Plus® contains carrageenan, citric acid, methylparaben,
microcrystalline cellulose, carboxymethylcellulose sodium, potassium sorbate,
simethicone, sodium phosphate monobasic, xanthan gum, and water. Ora-Sweet®
contains citric acid, berry citrus flavorant, glycerin, methylparaben, potassium
sorbate, sodium phosphate monobasic, sorbitol, sucrose, and water.
Contraindications
CONTRAINDICATIONS
Benazepril hydrochloride is contraindicated in patients who are
hypersensitive to this product or to any other ACE inhibitor.
Benazepril hydrochloride is also contraindicated in patients with a history
of angioedema with or without previous ACE inhibitor treatment
Warnings
WARNINGS
Anaphylactoid and Possibly Related Reactions
Presumably because angiotensin-converting enzyme inhibitors affect the
metabolism of eicosanoids and polypeptides, including endogenous bradykinin,
patients receiving ACE inhibitors (including Benazepril hydrochloride) may be
subject to a variety of adverse reactions, some of them serious.
Head and Neck Angioedema: Angioedema of the
face, extremities, lips, tongue, glottis, and larynx has been reported in
patients treated with angiotensin-converting enzyme inhibitors. In U.S. clinical
trials, symptoms consistent with angioedema were seen in none of the subjects
who received placebo and in about 0.5% of the subjects who received Benazepril
hydrochloride. Angioedema associated with laryngeal edema can be fatal. If
laryngeal stridor or angioedema of the face, tongue, or glottis occurs,
treatment with benazepril hydrochloride should be discontinued and appropriate
therapy instituted immediately. Where there is involvement of
the tongue, glottis, or larynx, likely to cause airway obstruction, appropriate
therapy, e.g., subcutaneous epinephrine injection 1:1000 (0.3 mL to 0.5 mL)
should be promptly administered (see
ADVERSE REACTIONS
).
Intestinal Angioedema: Intestinal angioedema
has been reported in patients treated with ACE inhibitors. These patients
presented with abdominal pain (with or without nausea or vomiting); in some
cases there was not prior history of facial angioedema and C-1 esterase levels
were normal. The angioedema was diagnosed by procedures including abdominal CT
scan or ultrasound, or at surgery, and symptoms resolved after stopping the ACE
inhibitor. Intestinal angioedema should be included in the differential
diagnosis of patients on ACE inhibitors presenting with abdominal pain.
Anaphylactoid Reactions During
Desensitization: Two patients undergoing desensitizing treatment with
hymenoptera venom while receiving ACE inhibitors sustained life-threatening
anaphylactoid reactions. In the same patients, these reactions were avoided when
ACE inhibitors were temporarily withheld, but they reappeared upon inadvertent
rechallenge.
Anaphylactoid Reactions During Membrane
Exposure: Anaphylactoid reactions have been reported in patients dialyzed
with high-flux membranes and treated concomitantly with an ACE inhibitor.
Anaphylactoid reactions have also been reported in patients undergoing
low-density lipoprotein apheresis with dextran sulfate absorption (a procedure
dependent upon devices not approved in the United States).
Hypotension
Benazepril hydrochloride can cause symptomatic hypotension. Like other ACE
inhibitors, benazepril has been only rarely associated with hypotension in
uncomplicated hypertensive patients. Symptomatic hypotension is most likely to
occur in patients who have been volume- and/or salt-depleted as a result of
prolonged diuretic therapy, dietary salt restriction, dialysis, diarrhea, or
vomiting. Volume- and/or salt-depletion should be corrected before initiating
therapy with Benazepril hydrochloride.
In patients with congestive heart failure, with or without associated renal
insufficiency, ACE inhibitor therapy may cause excessive hypotension, which may
be associated with oliguria or azotemia and, rarely, with acute renal failure
and death. In such patients, benazepril hydrochloride therapy should be started
under close medical supervision; they should be followed closely for the first 2
weeks of treatment and whenever the dose of benazepril or diuretic is
increased.
If hypotension occurs, the patient should be placed in a supine position,
and, if necessary, treated with intravenous infusion of physiological saline.
Benazepril hydrochloride treatment usually can be continued following
restoration of blood pressure and volume.
Neutropenia/Agranulocytosis
Another angiotensin-converting enzyme inhibitor, captopril, has been shown to
cause agranulocytosis and bone marrow depression, rarely in uncomplicated
patients, but more frequently in patients with renal impairment, especially if
they also have a collagen-vascular disease such as systemic lupus erythematosus
or scleroderma. Available data from clinical trials of benazepril are
insufficient to show that benazepril does not cause agranulocytosis at similar
rates. Monitoring of white blood cell counts should be considered in patients
with collagen-vascular disease, especially if the disease is associated with
impaired renal function.
Fetal/Neonatal Morbidity and Mortality
ACE inhibitors can cause fetal and neonatal morbidity and death when
administered to pregnant women. Several dozen cases have been reported in the
world literature. When pregnancy is detected, Benazepril hydrochloride should be
discontinued as soon as possible and monitoring of the fetal development should
be performed on a regular basis.
The use of ACE inhibitors during the second and third trimesters of pregnancy
has been associated with fetal and neonatal injury, including hypotension,
neonatal skull hypoplasia, anuria, reversible or irreversible renal failure, and
death. Oligohydramnios has also been reported, presumably resulting from
decreased fetal renal function; oligohydramnios in this setting has been
associated with fetal limb contractures, craniofacial deformation, and
hypoplastic lung development. Prematurity, intrauterine growth retardation, and
patent ductus arteriosus have also been reported, although it is not clear
whether these occurrences were due to the ACE inhibitor exposure.
In addition, use of ACE inhibitors during the first trimester of pregnancy
has been associated with a potentially increased risk of birth defects. In women
planning to become pregnant, ACE inhibitors (including Benazepril hydrochloride)
should not be used. Women of childbearing age should be made aware of the
potential risk and ACE inhibitors (including Benazepril hydrochloride) should
only be given after careful counseling and consideration of individual risks and
benefits.
Rarely (probably less often than once in every thousand pregnancies), no
alternative to ACE inhibitors will be found. In these rare cases, the mothers
should be apprised of the potential hazards to their fetuses, and serial
ultrasound examinations should be performed to assess the intraamniotic
environment.
If oligohydramnios is observed, benazepril should be discontinued unless it
is considered life-saving for the mother. Contraction stress testing (CST), a
nonstress test (NST), or biophysical profiling (BPP) may be appropriate,
depending upon the week of pregnancy. Patients and physicians should be aware,
however, that oligohydramnios may not appear until after the fetus has sustained
irreversible injury.
Infants with histories of in utero exposure to ACE inhibitors should be
closely observed for hypotension, oliguria, and hyperkalemia. If oliguria
occurs, attention should be directed toward support of blood pressure and renal
perfusion. Exchange transfusion or dialysis may be required as means of
reversing hypotension and/or substituting for disordered renal function.
Benazepril, which crosses the placenta, can theoretically be removed from the
neonatal circulation by these means; there are occasional reports of benefit
from these maneuvers with another ACE inhibitor, but experience is limited.
No teratogenic effects of benazepril hydrochloride were seen in studies of
pregnant rats, mice, and rabbits. On a mg/m2 basis, the doses used in these
studies were 60 times (in rats), 9 times (in mice), and more than 0.8 times (in
rabbits) the maximum recommended human dose (assuming a 50-kg woman). On a mg/kg
basis these multiples are 300 times (in rats), 90 times (in mice), and more than
3 times (in rabbits) the maximum recommended human dose.
Hepatic
Failure
Rarely, ACE inhibitors have been associated with a syndrome that starts with
cholestatic jaundice and progresses to fulminant hepatic necrosis and
(sometimes) death. The mechanism of this syndrome is not understood. Patients
receiving ACE inhibitors who develop jaundice or marked elevations of hepatic
enzymes should discontinue the ACE inhibitor and receive appropriate medical
follow-up.
PRECAUTIONS
General
Impaired Renal Function: As a consequence of
inhibiting the renin-angiotensin-aldosterone system, changes in renal function
may be anticipated in susceptible individuals. In patients with severe
congestive heart failure whose renal function may depend on the activity of the
renin-angiotensin-aldosterone system, treatment with angiotensin-converting
enzyme inhibitors, including benazepril hydrochloride, may be associated with
oliguria and/or progressive azotemia and (rarely) with acute renal failure
and/or death. In a small study of hypertensive patients with renal artery
stenosis in a solitary kidney or bilateral renal artery stenosis, treatment with
benazepril hydrochloride was associated with increases in blood urea nitrogen
and serum creatinine; these increases were reversible upon discontinuation of
Benazepril hydrochloride or diuretic therapy, or both. When such patients are
treated with ACE inhibitors, renal function should be monitored during the first
few weeks of therapy. Some hypertensive patients with no apparent preexisting
renal vascular disease have developed increases in blood urea nitrogen and serum
creatinine, usually minor and transient, especially when Benazepril
hydrochloride has been given concomitantly with a diuretic. This is more likely
to occur in patients with preexisting renal impairment. Dosage reduction of
Benazepril hydrochloride and/or discontinuation of the diuretic may be required.
Evaluation of the hypertensive patient should always include
assessment of renal function (see
DOSAGE AND ADMINISTRATION
).
Hyperkalemia: In clinical trials, hyperkalemia
(serum potassium at least 0.5 mEq/L greater than the upper limit of normal)
occurred in approximately 1% of hypertensive patients receiving benazepril
hydrochloride. In most cases, these were isolated values which resolved despite
continued therapy. Risk factors for the development of hyperkalemia include
renal insufficiency, diabetes mellitus, and the concomitant use of
potassium-sparing diuretics, potassium supplements, and/or potassium-containing
salt substitutes, which should be used cautiously, if at all, with Benazepril
hydrochloride (see Drug
Interactions ).
Cough: Presumably due to the inhibition of the
degradation of endogenous bradykinin, persistent nonproductive cough has been
reported with all ACE inhibitors, always resolving after discontinuation of
therapy. ACE inhibitor-induced cough should be considered in the differential
diagnosis of cough.
Impaired Liver Function: In patients with
hepatic dysfunction due to cirrhosis, levels of benazeprilat are essentially
unaltered (see WARNINGS, Hepatic
Failure ).
Surgery/Anesthesia: In patients undergoing
surgery or during anesthesia with agents that produce hypotension, benazepril
will block the angiotensin II formation that could otherwise occur secondary to
compensatory renin release. Hypotension that occurs as a result of this
mechanism can be corrected by volume expansion.
Adverse reactions
Benazepril hydrochloride has been evaluated for safety in over
6000 patients with hypertension; over 700 of these patients were treated for at
least one year. The overall incidence of reported adverse events was comparable
in Benazepril hydrochloride and placebo patients.
How supplied
HOW SUPPLIED
Benazepril Hydrochloride Tablets, USP are supplied as
follows:
5 mg (white biconvex, round, uncoated tablets, debossed with “51” on one side
and “A” on the other side)
Bottles of 30: NDC 65162-751-03
Bottles of 100: NDC 65162-751-10
Bottles of 500: NDC 65162-751-50
10 mg (white biconvex, round, uncoated tablets, debossed with “52” on one
side and “A” on the other side)
Bottles of 30: NDC 65162-752-03
Bottles of 100: NDC 65162-752-10
Bottles of 500: NDC 65162-752-50
20 mg (white biconvex, round, uncoated tablets, debossed with “53” on one
side and “A” on the other side)
Bottles of 30: NDC 65162-753-03
Bottles of 100: NDC 65162-753-10
Bottles of 500: NDC 65162-753-50
40 mg (white biconvex, round, uncoated tablets, debossed with “54” on one
side and “A” on the other side)
Bottles of 30: NDC 65162-754-03
Bottles of 100: NDC 65162-754-10
Bottles of 500: NDC 65162-754-50
Store at 20º to 25°C (68° to 77ºF) (see USP Controlled Room Temperature)
Dispense in tight container (USP).
Manufactured by:
Amneal Pharmaceuticals of NY
Hauppauge, NY 11788
Distributed by
Amneal Pharmaceuticals
Glasgow, KY 42141
Rev. 12-2009
Clinical pharmacology
CLINICAL PHARMACOLOGY
Mechanism of Action
Benazepril and benazeprilat inhibit angiotensin-converting enzyme (ACE) in
human subjects and animals. ACE is a peptidyl dipeptidase that catalyzes the
conversion of angiotensin I to the vasoconstrictor substance, angiotensin II.
Angiotensin II also stimulates aldosterone secretion by the adrenal cortex.
Inhibition of ACE results in decreased plasma angiotensin II, which leads to
decreased vasopressor activity and to decreased aldosterone secretion. The
latter decrease may result in a small increase of serum potassium. Hypertensive
patients treated with Benazepril hydrochloride alone for up to 52 weeks had
elevations of serum potassium of up to 0.2 mEq/L. Similar patients treated with
Benazepril hydrochloride and hydrochlorothiazide for up to 24 weeks had no
consistent changes in their serum potassium (see PRECAUTIONS ).
Removal of angiotensin II negative feedback on renin secretion leads to
increased plasma renin activity. In animal studies, benazepril had no inhibitory
effect on the vasopressor response to angiotensin II and did not interfere with
the hemodynamic effects of the autonomic neurotransmitters acetylcholine,
epinephrine, and norepinephrine.
ACE is identical to kininase, an enzyme that degrades bradykinin. Whether
increased levels of bradykinin, a potent vasodepressor peptide, play a role in
the therapeutic effects of benazepril hydrochloride remains to be
elucidated.
While the mechanism through which benazepril lowers blood pressure is
believed to be primarily suppression of the renin-angiotensin-aldosterone
system, benazepril has an antihypertensive effect even in patients with
low-renin hypertension (see INDICATIONS AND USAGE ).
Pharmacokinetics and Metabolism
Following oral administration of benazepril hydrochloride, peak plasma
concentrations of benazepril are reached within 0.5-1.0 hours. The extent of
absorption is at least 37% as determined by urinary recovery and is not
significantly influenced by the presence of food in the GI tract.
Cleavage of the ester group (primarily in the liver) converts benazepril to
its active metabolite, benazeprilat. Peak plasma concentrations of benazeprilat
are reached 1-2 hours after drug intake in the fasting state and 2-4 hours after
drug intake in the nonfasting state. The serum protein binding of benazepril is
about 96.7% and that of benazeprilat about 95.3%, as measured by equilibrium
dialysis; on the basis of in vitro studies, the degree of protein binding should
be unaffected by age, hepatic dysfunction, or concentration (over the
concentration range of 0.24-23.6 µmol/L).
Benazepril is almost completely metabolized to benazeprilat, which has much
greater ACE inhibitory activity than benazepril, and to the glucuronide
conjugates of benazepril and benazeprilat. Only trace amounts of an administered
dose of benazepril hydrochloride can be recovered in the urine as unchanged
benazepril, while about 20% of the dose is excreted as benazeprilat, 4% as
benazepril glucuronide, and 8% as benazeprilat glucuronide.
The kinetics of benazepril are approximately dose-proportional within the
dosage range of 10-80 mg.
In adults, the effective half-life of accumulation
of benazeprilat following multiple dosing of benazepril hydrochloride is 10-11
hours. Thus, steady-state concentrations of benazeprilat should be reached after
2 or 3 doses of benazepril hydrochloride given once daily.
The kinetics did not change, and there was no significant accumulation during
chronic administration (28 days) of once-daily doses between 5 mg and 20 mg.
Accumulation ratios based on AUC and urinary recovery of benazeprilat were 1.19
and 1.27, respectively.
Benazepril and benazeprilat are cleared predominantly by renal excretion in
healthy subjects with normal renal function. Nonrenal (i.e., biliary) excretion
accounts for approximately 11%-12% of benazeprilat excretion in healthy
subjects. In patients with renal failure, biliary clearance may compensate to an
extent for deficient renal clearance.
In patients with renal insufficiency, the
disposition of benazepril and benazeprilat in patients with mild-to-moderate
renal insufficiency (creatinine clearance >30 mL/min) is similar to that in
patients with normal renal function. In patients with creatinine clearance ≤ 30
mL/min, peak benazeprilat levels and the initial (alpha phase) half-life
increase, and time to steady state may be delayed (see DOSAGE AND ADMINISTRATION ).
When dialysis was started two hours after ingestion of 10 mg of benazepril,
approximately 6% of benazeprilat was removed in 4 hours of dialysis. The parent
compound, benazepril, was not detected in the dialysate.
In patients with hepatic insufficiency (due to
cirrhosis), the pharmacokinetics of benazeprilat are essentially
unaltered. The pharmacokinetics of benazepril and benazeprilat do not appear to
be influenced by age.
In
pediatric patients, (N=45) hypertensive, age 6 to 16 years, given
multiple daily doses of Benazepril hydrochloride (0.1 to 0.5 mg/kg), the
clearance of benazeprilat for children 6 to 12 years old was 0.35 L/hr/kg, more
than twice that of healthy adults receiving a single dose of 10 mg (0.13
L/hr/kg). In adolescents, it was 0.17 L/hr/kg, 27% higher than that of healthy
adults. The terminal elimination half-life of benazeprilat in pediatric patients
was around 5 hours, one third that observed in adults.
Pharmacodynamics
Single and multiple doses of 10 mg or more of benazepril hydrochloride cause
inhibition of plasma ACE activity by at least 80%-90% for at least 24 hours
after dosing. Pressor responses to exogenous angiotensin I were inhibited by
60%-90% (up to 4 hours post-dose) at the 10-mg dose.
Hypertension
Adult
Administration of benazepril hydrochloride to patients with mild-to-moderate
hypertension results in a reduction of both supine and standing blood pressure
to about the same extent with no compensatory tachycardia. Symptomatic postural
hypotension is infrequent, although it can occur in patients who are salt-
and/or volume-depleted (see WARNINGS ).
In single-dose studies, benazepril hydrochloride lowered blood pressure
within 1 hour, with peak reductions achieved 2-4 hours after dosing. The
antihypertensive effect of a single dose persisted for 24 hours. In
multiple-dose studies, once-daily doses of 20-80 mg decreased seated pressure
(systolic/diastolic) 24 hours after dosing by about 6 -12 /4-7 mmHg. The trough
values represent reductions of about 50% of that seen at peak.
Four dose-response studies using once-daily dosing were conducted in 470
mild-to-moderate hypertensive patients not using diuretics. The minimal
effective once-daily dose of benazepril hydrochloride was 10 mg; but further
falls in blood pressure, especially at morning trough, were seen with higher
doses in the studied dosing range (10-80 mg). In studies comparing the same
daily dose of benazepril hydrochloride given as a single morning dose or as a
twice-daily dose, blood pressure reductions at the time of morning trough blood
levels were greater with the divided regimen.
During chronic therapy, the maximum reduction in blood pressure with any dose
is generally achieved after 1-2 weeks. The antihypertensive effects of
benazepril hydrochloride have continued during therapy for at least two years.
Abrupt withdrawal of benazepril hydrochloride has not been associated with a
rapid increase in blood pressure.
In patients with mild-to-moderate hypertension, Benazepril hydrochloride
10-20 mg was similar in effectiveness to captopril, hydrochlorothiazide,
nifedipine SR, and propranolol. The antihypertensive effects of Benazepril
hydrochloride were not appreciably different in patients receiving high- or
low-sodium diets.
In hemodynamic studies in dogs, blood pressure reduction was accompanied by a
reduction in peripheral arterial resistance, with an increase in cardiac output
and renal blood flow and little or no change in heart rate. In normal human
volunteers, single doses of benazepril caused an increase in renal blood flow
but had no effect on glomerular filtration rate.
Use of Benazepril hydrochloride in combination with thiazide diuretics gives
a blood-pressure-lowering effect greater than that seen with either agent alone.
By blocking the renin-angiotensin-aldosterone axis, administration of Benazepril
hydrochloride tends to reduce the potassium associated with the diuretic.
Pediatric
In a clinical study of 107 pediatric patients, 7 to 16 years of age, with
either systolic or diastolic pressure above the 95th percentile, patients were
given 0.1 or 0.2 mg/kg then titrated up to 0.3 or 0.6 mg/kg with a maximum dose
of 40 mg once daily. After four weeks of treatment, the 85 patients whose blood
pressure was reduced on therapy were then randomized to either placebo or
benazepril and were followed up for an additional two weeks. At the end of two
weeks, blood pressure (both systolic and diastolic) in children withdrawn to
placebo rose by 4 to 6 mmHg more than in children on benazepril. No
dose-response was observed for the three doses.
Package label
BENAZEPRIL 20MG LABEL
BENAZEPRIL 20MG LABEL
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