However, this article should not be used as a substitute for the knowledge and expertise of a licensed healthcare professional. You should always consult your doctor or another healthcare professional before taking any medication. The drug information contained herein is subject to change and is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects.
The absence of warnings or other information for a given drug does not indicate that the drug or drug combination is safe, effective, or appropriate for all patients or all specific uses. Read the article in Spanish.
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Medically reviewed by Brenda B. Spriggs, M. Fifteen good foods for high blood pressure. Medically reviewed by Natalie Butler, R. Can essential oils help lower hypertension? Medically reviewed by Debra Rose Wilson, Ph. In terms of blood pressure lowering, both HCTZ and chlorthalidone appear to be very effective. Head-to-head studies have shown trends favoring chlorthalidone as a more effective blood pressure lowering agent compared with HCTZ, but statistical significance in this regard has not been consistently demonstrated.
Also unclear is the relative benefits of these 2 drugs with regards to reducing clinical complications of hypertension, namely cardiovascular morbidity and mortality. In patients with renal failure, biliary clearance may compensate to an extent for deficient renal clearance. Following oral administration, plasma hydrochlorothiazide concentrations decline bi-exponentially, with a mean distribution half-life of about 2 hours and an elimination half-life of about 10 hours.
In normal human volunteers, single doses of benazepril caused an increase in renal blood flow but had no effect on glomerular filtration rate.
After oral administration of hydrochlorothiazide, diuresis begins within 2 hours, peaks in about 4 hours and lasts about 6 to 12 hours. Benazepril hydrochloride and hydrochlorothiazide potentiates the antihypertensive action of other antihypertensive drugs e.
In single-dose studies, benazepril lowered blood pressure within 1 hour, with peak reductions achieved 2 to 4 hours after dosing. The antihypertensive effect of a single dose persisted for 24 hours. Four dose-response studies of benazepril monotherapy using once-daily dosing were conducted in mild-to-moderate hypertensive patients not using diuretics.
The minimal effective once-daily dose of benazepril was 10 mg; further falls in blood pressure, especially at morning trough, were seen with higher doses in the studied dosing range 10 mg to 80 mg.
In studies comparing the same daily dose of benazepril 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. The antihypertensive effects of benazepril were not appreciably different in patients receiving high- or low-sodium diets.
In 15 controlled clinical trials, healthy or hypertensive patients were exposed to benazepril and hydrochlorothiazide of which were exposed for at least 6 months, for at least 12 months and 25 for at least 24 months. Although benazepril monotherapy is somewhat less effective in blacks than in nonblacks, the efficacy of combination therapy appears to be independent of race. Benazepril hydrochloride and hydrochlorothiazide tablets are indicated for the treatment of hypertension.
Benazepril hydrochloride and hydrochlorothiazide is contraindicated in patients who are anuric. Benazepril hydrochloride and hydrochlorothiazide is also contraindicated in patients who are hypersensitive to benazepril, to any other ACE inhibitor, to hydrochlorothiazide, or to other sulfonamide-derived drugs. Hypersensitivity reactions are more likely to occur in patients with a history of allergy or bronchial asthma. Benazepril hydrochloride and hydrochlorothiazide is also contraindicated in patients with a history of angioedema with or without previous ACE inhibitor treatment.
Benazepril hydrochloride and hydrochlorothiazide is contraindicated in combination with a neprilysin inhibitor e. Do not coadminister aliskiren with angiotensin receptor blockers, ACE inhibitors, including benazepril hydrochloride and hydrochlorothiazide in patients with diabetes.
Presumably because angiotensin-converting enzyme inhibitors affect the metabolism of eicosanoids and polypeptides, including endogenous bradykinin, patients receiving ACE inhibitors including benazepril may be subject to a variety of adverse reactions, some of them serious. Angioedema of the face, extremities, lips, tongue, glottis, and larynx has been reported in patients treated with angiotensin-converting enzyme inhibitors.
Angioedema associated with laryngeal edema can be fatal. If laryngeal stridor or angioedema of the face, tongue, or glottis occurs, treatment with benazepril hydrochloride and hydrochlorothiazide should be discontinued and appropriate therapy instituted immediately. When involvement of the tongue, glottis, or larynx appears likely to cause airway obstruction, appropriate therapy, e.
Black patients receiving ACE inhibitors have been reported to have a higher incidence of angioedema compared to nonblacks. 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 no 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.
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 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. Hypersensitivity reactions to hydrochlorothiazide are more likely in patients with allergy and asthma. Benazepril hydrochloride and hydrochlorothiazide can cause symptomatic hypotension.
Like other ACE inhibitors, benazepril has been only rarely associated with hypotension in uncomplicated hypertensive patients. Benazepril hydrochloride and hydrochlorothiazide should be used cautiously in patients receiving concomitant therapy with other antihypertensives.
The thiazide component of benazepril hydrochloride and hydrochlorothiazide may potentiate the action of other antihypertensive drugs, especially ganglionic or peripheral adrenergic-blocking drugs. The antihypertensive effects of the thiazide component may also be enhanced in the postsympathectomy patient.
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, azotemia, and rarely with acute renal failure and death. In such patients, benazepril hydrochloride and hydrochlorothiazide 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 and hydrochlorothiazide treatment usually can be continued following restoration of blood pressure and volume. Monitor renal function periodically in patients treated with benazepril hydrochloride and hydrochlorothiazide. Changes in renal function including acute renal failure can be caused by drugs that inhibit the renin-angiotensin system and by diuretics.
Patients whose renal function may depend in part on the activity of the renin-angiotensin system e. Consider withholding or discontinuing therapy in patients who develop a clinically significant decrease in renal function on benazepril hydrochloride and hydrochlorothiazide.
In a small study of hypertensive patients with unilateral or bilateral renal artery stenosis , treatment with benazepril was associated with increases in blood urea nitrogen and serum creatinine; these increases were reversible upon discontinuation of benazepril therapy, concomitant diuretic therapy, or both. Another angiotensin-converting enzyme inhibitor, captopril, has been shown to cause agranulocytosis and bone marrow depression, rarely in uncomplicated patients incidence probably less than once per 10, exposures but more frequently incidence possibly as great as once per exposures in patients with renal impairment, especially those who also have collagen-vascular diseases 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.
Use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death.
Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. Potential neonatal adverse effects include skull hypoplasia, anuria, hypotension, renal failure, and death. These adverse outcomes are usually associated with use of these drugs in the second and third trimester of pregnancy. Most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in the first trimester have not distinguished drugs affecting the renin-angiotensin system from other antihypertensive agents.
Appropriate management of maternal hypertension during pregnancy is important to optimize outcomes for both mother and fetus. In the unusual case that there is no appropriate alternative to therapy with drugs affecting the renin-angiotensin system for a particular patient, apprise the mother of the potential risk to the fetus.
Perform serial ultrasound examinations to assess the intra-amniotic environment. If oligohydramnios is observed, discontinue benazepril hydrochloride and hydrochlorothiazide unless it is considered life saving for the mother. Fetal testing may be appropriate, based on the week of pregnancy. Patients and physicians should be aware, however, that oligohydramnios may not appear until after the fetus has sustained irreversible injury.
No teratogenic effects of benazepril hydrochloride were seen in studies of pregnant rats, mice, and rabbits. Thiazides can cross the placenta, and concentrations reached in the umbilical vein approach those in the maternal plasma. Hydrochlorothiazide, like other diuretics, can cause placental hypoperfusion.
It accumulates in the amniotic fluid, with reported concentrations up to 19 times higher than in umbilical vein plasma. Use of thiazides during pregnancy is associated with a risk of fetal or neonatal jaundice or thrombocytopenia. Since they do not prevent or alter the course of EPH Edema, Proteinuria, Hypertension gestosis pre-eclampsia , these drugs must not be used to treat hypertension in pregnant women.
The use of hydrochlorothiazide for other indications e. 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. Thiazide diuretics have been reported to cause exacerbation or activation of systemic lupus erythematosus. Hydrochlorothiazide, a sulfonamide, can cause an idiosyncratic reaction, resulting in acute transient myopia and acute angle-closure glaucoma.
Symptoms include acute onset of decreased visual acuity or ocular pain and typically occur within hours to weeks of drug initiation. Benazepril and hydrochlorothiazide controls high blood pressure but does not cure it. Continue to take benazepril and hydrochlorothiazide even if you feel well.
Do not stop taking benazepril and hydrochlorothiazide without talking to your doctor. This medication may be prescribed for other uses; ask your doctor or pharmacist for more information.
Talk to your doctor before using salt substitutes containing potassium. If your doctor prescribes a low-salt or low-sodium diet, or an exercise program, follow these directions carefully. Take the missed dose as soon as you remember it. However, if it is almost time for the next dose, skip the missed dose and continue your regular dosing schedule.
Do not take a double dose to make up for a missed one. Benazepril and hydrochlorothiazide may cause other side effects. Call your doctor if you have any unusual problems while taking this medication. Keep this medication in the container it came in, tightly closed, and out of reach of children. Store it at room temperature and away from excess heat and moisture not in the bathroom. Unneeded medications should be disposed of in special ways to ensure that pets, children, and other people cannot consume them.
However, you should not flush this medication down the toilet. Instead, the best way to dispose of your medication is through a medicine take-back program.
It is important to keep all medication out of sight and reach of children as many containers such as weekly pill minders and those for eye drops, creams, patches, and inhalers are not child-resistant and young children can open them easily.
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