Prent

Prent Uses, Dosage, Side Effects, Food Interaction and all others data.

A cardioselective beta-adrenergic antagonist with little effect on the bronchial receptors. The drug has stabilizing and quinidine-like effects on cardiac rhythm as well as weak inherent sympathomimetic action.

Prent is a cardioselective, beta-adrenoreceptor blocking agent, which possesses mild intrinsic sympathomimetic activity (ISA) in its therapeutically effective dose range. In general, beta-blockers reduce the work the heart has to do and allow it to beat more regularly. Prent has less antagonistic effects on peripheral vascular ß2-receptors at rest and after epinephrine stimulation than nonselective beta-antagonists. Low doses of acebutolol produce less evidence of bronchoconstriction than nonselective agents like propranolol but more than atenolol.

Trade Name Prent
Availability Prescription only
Generic Acebutolol
Acebutolol Other Names Acebutolol, Acebutololum, Acetobutolol
Related Drugs amlodipine, lisinopril, metoprolol, losartan, furosemide, hydrochlorothiazide, bisoprolol, sotalol, magnesium sulfate, Zebeta
Type
Formula C18H28N2O4
Weight Average: 336.4259
Monoisotopic: 336.204907394
Protein binding

26%

Groups Approved, Investigational
Therapeutic Class
Manufacturer
Available Country
Last Updated: September 19, 2023 at 7:00 am
Prent
Prent

Uses

Prent is a selective β1-receptor antagonist used for the management of hypertension and ventricular premature beats in adults.

For the management of hypertension and ventricular premature beats in adults.

Prent is also used to associated treatment for these conditions: Chronic Stable Angina Pectoris, High Blood Pressure (Hypertension), Arrhythmia of ventricular origin

How Prent works

Prent is a selective β1-receptor antagonist. Activation of β1-receptors by epinephrine increases the heart rate and the blood pressure, and the heart consumes more oxygen. Prent blocks these receptors, lowering the heart rate and blood pressure. This drug then has the reverse effect of epinephrine. In addition, beta blockers prevent the release of renin, which is a hormone produced by the kidneys which leads to constriction of blood vessels.

Toxicity

Symptoms of overdose include extreme bradycardia, advanced atrioventricular block, intraventricular conduction defects, hypotension, severe congestive heart failure, seizures, and in susceptible patients, bronchospasm, and hypoglycemia.

Food Interaction

  • Take with or without food. Food decreases absorption rate and maximum concentration, but not to a clinically significant extent.

Prent Alcohol interaction

[Moderate]

Many psychotherapeutic and CNS-active agents (e.g., anxiolytics, sedatives, hypnotics, antidepressants, antipsychotics, opioids, alcohol, muscle relaxants) exhibit hypotensive effects, especially during initiation of therapy and dose escalation.

Coadministration with antihypertensives and other hypotensive agents, in particular vasodilators and alpha-blockers, may result in additive effects on blood pressure and orthostasis.

Caution and close monitoring for development of hypotension is advised during coadministration of these agents.

Some authorities recommend avoiding alcohol in patients receiving vasodilating antihypertensive drugs.

Patients should be advised to avoid rising abruptly from a sitting or recumbent position and to notify their physician if they experience dizziness, lightheadedness, syncope, orthostasis, or tachycardia.

Prent Cholesterol interaction

[Moderate] Beta-adrenergic receptor blocking agents (aka beta-blockers) may alter serum lipid profiles.

Increases in serum VLDL and LDL cholesterol and triglycerides, as well as decreases in HDL cholesterol, have been reported with some beta-blockers.

Patients with preexisting hyperlipidemia may require closer monitoring during beta-blocker therapy, and adjustments made accordingly in their lipid-lowering regimen.

Prent multivitamins interaction

[Moderate] ADJUST DOSING INTERVAL: Concurrent administration with calcium salts may decrease the oral bioavailability of atenolol and possibly other beta-blockers.

The exact mechanism of interaction is unknown.

In six healthy subjects, calcium 500 mg (as lactate, carbonate, and gluconate) reduced the mean peak plasma concentration (Cmax) and area under the concentration-time curve (AUC) of atenolol (100 mg) by 51% and 32%, respectively.

The elimination half-life increased by 44%.

Twelve hours after the combination, beta-blocking activity (as indicated by inhibition of exercise tachycardia) was reduced compared to that with atenolol alone.

However, during a 4-week treatment in six hypertensive patients, there was no difference in blood pressure values between treatments.

The investigators suggest that prolongation of the elimination half-life induced by calcium coadministration may have led to atenolol cumulation during long-term dosing, which compensated for the reduced bioavailability.

It may help to separate the administration times of beta-blockers and calcium products by at least 2 hours.

Patients should be monitored for potentially diminished beta-blocking effects following the addition of calcium therapy.

Elimination Route

Well absorbed from the Gl tract with an absolute bioavailability of approximately 40% for the parent compound. In

Half Life

The plasma elimination half-life is approximately 3 to 4 hours. The half-life of its metabolite, diacetolol, is 8 to 13 hours.

Elimination Route

Elimination via renal excretion is approximately 30% to 40% and by non-renal mechanisms 50% to 60%, which includes excretion into the bile and direct passage through the intestinal wall.

Innovators Monograph

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*** Taking medicines without doctor's advice can cause long-term problems.
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