Stereochemistry | RACEMIC |
Molecular Formula | C16H21NO2.C12H24O2 |
Molecular Weight | 459.6612 |
Optical Activity | ( + / - ) |
Defined Stereocenters | 0 / 1 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CCCCCCCCCCCC(O)=O.CC(C)NCC(O)COC1=C2C=CC=CC2=CC=C1
InChI
InChIKey=CAWRJDLZCQEKMX-UHFFFAOYSA-N
InChI=1S/C16H21NO2.C12H24O2/c1-12(2)17-10-14(18)11-19-16-9-5-7-13-6-3-4-8-15(13)16;1-2-3-4-5-6-7-8-9-10-11-12(13)14/h3-9,12,14,17-18H,10-11H2,1-2H3;2-11H2,1H3,(H,13,14)
Propranolol is a nonselective, beta-adrenergic receptor-blocking agent possessing no other autonomic nervous system activity. At dosages greater than required for beta blockade, propranolol also exerts a quinidine-like or anesthetic-like membrane action, which affects the cardiac action potential. Among the factors that may be involved in contributing to the antihypertensive action include: (1) decreased cardiac output, (2) inhibition of renin release by the kidneys, and (3) diminution of tonic sympathetic nerve outflow from vasomotor centers in the brain. Although total peripheral resistance may increase initially, it readjusts to or below the pretreatment level with chronic use of propranolol. Effects of propranolol on plasma volume appear to be minor and somewhat variable. In angina pectoris, propranolol generally reduces the oxygen requirement of the heart at any given level of effort by blocking the catecholamine-induced increases in the heart rate, systolic blood pressure, and the velocity and extent of myocardial contraction. Propranolol may increase oxygen requirements by increasing left ventricular fiber length, end diastolic pressure, and systolic ejection period. The net physiologic effect of beta-adrenergic blockade is usually advantageous and is manifested during exercise by delayed onset of pain and increased work capacity. Propranolol exerts its antiarrhythmic effects in concentrations associated with beta-adrenergic blockade, and this appears to be its principal antiarrhythmic mechanism of action. In dosages greater than required for beta blockade, propranolol also exerts a quinidine-like or anesthetic-like membrane action, which affects the cardiac action potential. The significance of the membrane action in the treatment of arrhythmias is uncertain. The mechanism of the anti-migraine effect of propranolol has not been established. Propranolol is indicated in the management of hypertension. It may be used alone or used in combination with other antihypertensive agents, particularly a thiazide diuretic. Also is indicated to decrease angina frequency and increase exercise tolerance in patients with angina pectoris; for the prophylaxis of common migraine headache. In addition, is used to improve NYHA functional class in symptomatic patients with hypertrophic subaortic stenosis. Due to the high penetration across the blood–brain barrier, propranolol causes sleep disturbances such as insomnia and vivid dreams, and nightmares. Dreaming (rapid eye movement sleep, REM) was reduced and increased awakening.
CNS Activity
Originator
Approval Year
Cmax
Overview
CYP3A4 | CYP2C9 | CYP2D6 | hERG |
---|---|---|---|
OverviewOther
Other Inhibitor | Other Substrate | Other Inducer |
---|---|---|
Drug as perpetrator
Drug as victim
Tox targets
Sourcing
Sample Use Guides
Hypertension: The usual initial dosage is 80 mg capsules once daily, whether used alone or added to a diuretic. The dosage may be increased to 120 mg once.
Angina Pectoris: Starting with 80 mg capsules once daily, dosage
should be gradually increased at three- to seven-day intervals until optimal response is obtained. Although individual patients may respond at any dosage level, the average optimal dosage appears to be 160 mg once daily.
Migraine: The initial oral dose is 80 mg capsules once daily. The usual effective dose range is 160 to 240 mg once daily.
Hypertrophic Subaortic Stenosis: The usual dosage is 80 to 160 mg capsules once daily.
Route of Administration:
Oral