| Indication |
For the prophylaxis of migraine. |
| Pharmacodynamics |
Propranolol, the prototype of the beta-adrenergic receptor
antagonists, is a competitive, nonselective beta-blocker similar to
nadolol without intrinsic sympathomimetic activity. Propanolol is a
racemic compound; the l-isomer is responsible for adrenergic blocking
activity. |
| Mechanism of action |
Propranolol competes with sympathomimetic neurotransmitters such
as catecholamines for binding at beta(1)-adrenergic receptors in the
heart, inhibiting sympathetic stimulation. This results in a reduction
in resting heart rate, cardiac output, systolic and diastolic blood
pressure, and reflex orthostatic hypotension. |
| Absorption |
Propranolol is almost completely absorbed from the GI tract;
however, plasma concentrations attained are quite variable among
individuals. |
| Volume of distribution |
|
| Protein binding |
More than 90% |
| Metabolism |
Hepatic |
| Route of elimination |
Propranolol is extensively metabolized with most metabolites appearing in the urine. |
| Half life |
4 hours |
| Clearance |
Not Available |
| Toxicity |
Symptoms of overdose include bradycardia, cardiac failure, hypotension, and brochospasm. LD50=565 mg/kg (orally in mice). |
