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Propranolol has been studied most carefully in experiments and in clinics. It is used for ventricular tachycardia, arrhythmia caused by digitalis drug overdose, or as a result of thyrotoxosis or excess catecholamine activity. Despite the fact that there are a number of β-adrenoblockers, propranolol is considered the first choice of drugs although other blockers of calcium blockers can be just as effective.

Propranolol is used for treating hypertension, angina pectoris, supraventricular arrhythmia, ventricular tachycardia, migraines, hypertrophic subaortal stenosis, and pheochromocytosis. It is used following a myocardial infraction.

Propranolol is used in treating arterial hypertonicity, angina, extrasystole, superventricular arrhythmia, ventricular tachycardia, migraines, hypertrophic subaortic stenosis, and pheochromocytoma. It also is used in the postanginal phase of myocardial infarctions.

ChEBI: (R)-(+)-propranolol is a propranolol.

Propranolol slows heart rate, increases the effective refractory period of atrioventricular ganglia, suppresses automatism of heart cells, and reduces excitability and contractibility of the myocardium. It is used for supraventricular and ventricular arrhythmias.

Tetrahedron Letters, 31, p. 2157, 1990 DOI: 10.1016/0040-4039(90)80097-6

R(+)-PROPRANOLOL HCL(Inderal, others) is the prototypical andnonselective β-blocker. It blocks the β1- and β2-receptorswith equal affinity, lacks ISA, and does not block β-receptors. R(+)-PROPRANOLOL HCL like the other β-blockers discussed,is a competitive blocker whose receptor-blockingactions can be reversed with sufficient concentrations of β-agonists.

Less active enantiomer of the β -adrenoceptor antagonist propranolol ((RS)-1-[(1-Methylethyl)amino]-3-(1-naphthalenyloxy)-2-propanol hydrochloride ).

Propranolol is a nonselective β-adrenoblocker that affects both the mechanical and electrophysiological properties of the myocardium. It lowers myocardial contractibility, heart rate, blood pressure, and the myocardial need for oxygen. These properties make propranolol and other β-adrenoblockers useful antianginal drugs.

Currently, R(+)-PROPRANOLOL HCL is approved for use inthe United States for hypertension, cardiac arrhythmias,angina pectoris, postmyocardial infarction, hypertrophiccardiomyopathy, pheochromocytoma, migraine prophylaxis,and essential tremor. In addition, because of its highlipophilicity (log P=3.10) and thus its ability to penetratethe CNS, propranolol has found use in treating anxiety andis under investigation for the treatment of a variety of otherconditions, including schizophrenia, alcohol withdrawalsyndrome, and aggressive behavior.

The toxicity associated with propranolol is for the most part related to its primary pharmacological action, inhibition of the cardiac β-adrenoceptors. In addition, propranolol exerts direct cardiac depressant effects that become manifest when the drug is administered rapidly by the IV route.Glucagon immediately reverses all cardiac depressant effects of propranolol, and its use is associated with a minimum of side effects. The inotropic agents amrinone (Inocor) and milrinone (Primacor) provide alternative means of augmenting cardiac contractile function in the presence of β-adrenoceptor blockade. Propranolol may also stimulate bronchospasm in patients with asthma.
Since propranolol crosses the placenta and enters the fetal circulation, fetal cardiac responses to the stresses of labor and delivery will be blocked. Additionally, propranolol crosses the blood-brain barrier and is associated with mood changes and depression. School difficulties are commonly associated with its use in children. Propranolol may also cause hypoglycemia in infants.

Propranolol, 1-(iso-propylamino)-3-(1-naphthyloxy)-2-propanol (12.1.2), is synthesized in two ways from the same initial substance. The first way consists of reacting 1-naphthol with epichlorohydrin. Opening of the epoxide ring gives 1-chloro-3- (1-naphthyloxy)-2-propanol (12.1.1), which is reacted further with iso-propylamine, giving propranolol (12.1.2).

The second method uses the same reagents in the presence of a base and consists of initially making 3-(1-naphthyloxy)propylenoxide (12.1.3), the subsequent reaction with isopropylamine which results in epoxide ring opening leading to the formation of propranolol (12.1.2) [1–6].

Propranolol (Inderal) is suitable for both parental and oral administration. Absorption from the gastrointestinal tract is extensive. The peak therapeutic effect after oral administration occurs in 1 to 1.5 hours.The plasma half-life of propranolol is approximately 3 hours. The drug is concentrated in the lungs and to a lesser extent in the liver, brain, kidneys, and heart. Binding to plasma proteins is extensive (90%). The liver is the chief organ involved in the metabolism of propranolol, and the drug is subject to a significant degree of first-pass metabolism. At least eight metabolites have been recovered from the urine, the major excretory route.

Propranolol is contraindicated for patients with depressed myocardial function and may be contraindicated in the presence of digitalis toxicity because of the possibility of producing complete A-V block and ventricular asystole. Patients receiving anesthetic agents that tend to depress myocardial contractility (ether, halothane) should not receive propranolol. Propranolol should be used with extreme caution in patients with asthma. Up-regulation of β-receptors follows long-term therapy, making abrupt withdrawal of β-blockers dangerous for patients with ischemic heart disease.