Chemical formula: C₁₅H₂₃NO₃ Molecular mass: 265.348 g/mol PubChem compound: 4631
Oxprenolol is a non-selective, lipophilic betablocker exerting a sympatholytic effect and displaying mild to modest partial agonistic activity (PAA), also known as intrinsic sympathomimetic activity (ISA).
Drugs like oxprenolol with PAA cause comparatively less slowing of the resting heart rate and a less marked negative-inotropic effect than those without PAA. The risk of substantial bradycardia at rest and heart failure is lessened.
The antiarrhythmic effect of oxprenolol is primarily due to suppression of the arrhythmogenic sympathetic influence of catecholamines. Evidence that increased sympathetic stimulation predisposes to many arrhythmias is strong. This is supported by the increased incidence of arrhythmias in man in situations associated with high sympathetic drive or myocardial sensitisation to catecholamines e.g. exercise, emotional stress, phaeochromocytoma, trauma, myocardial ischaemia, anaesthesia, hyperthyroidism.
Oxprenolol decreases cardiac impulse formation in the sinus node with resultant slowing of the sinus rate; it slightly prolongs the sino-atrial conduction time; both the atrio-ventricular (AV) conduction time and the AV node refractory periods are lengthened.
Some beta-blockers such as oxprenolol possess a membrane stabilising activity (MSA) on the cardiac action potential, also known as “quinidine-like” or “local anaesthetic” action, a property that tends to result in greater cardiac depression than is seen with beta-blockers which do not have this pharmacological characteristic. However, at normal therapeutic doses, this property is probably clinically irrelevant and it only becomes manifest after overdose.
In coronary artery disease, oxprenolol is beneficial in increasing exercise tolerance and decreasing the frequency and severity of anginal attacks.
Emotional stress and anxiety states, the symptoms of which are largely caused by increased sympathetic drive, are alleviated by the sympatholytic effect of oxprenolol.
The exact way in which beta-blockers exert their antihypertensive action is still not fully understood. Various modes of action have been postulated. During chronic therapy the antihypertensive effect of beta-blockers is associated with a decline in peripheral resistance.
Oxprenolol is effective in lowering elevated supine, standing and exercise blood pressure; postural hypotension is unlikely to occur.
In the gastrointestinal tract, oral oxprenolol is rapidly and completely absorbed. Food has no significant effect on absorption. Peak plasma concentrations are achieved approximately 1 hour after drug administration.
Oxprenolol is subject to first-pass metabolism. Its systemic bioavailability is 20–70%.
Oxprenolol has a plasma-protein binding rate of approx. 80% and a calculated distribution volume of 1.2 l/kg.
Oxprenolol crosses the placental barrier. The concentration in the breast milk is equivalent to approx. 30% of that in the plasma.
Oxprenolol is moderately lipid-soluble and crosses the blood-brain barrier.
Oxprenolol has an elimination half-life of 1–2 hours. Oxprenolol is extensively metabolised, direct O-glucuronidation being the major metabolic pathway and oxidative reactions minor ones. Oxprenolol is excreted chiefly in the urine (almost exclusively in the form of inactive metabolites). The drug is not likely to accumulate.
Age has no effect on the pharmacokinetics of oxprenolol.
In patients with acute or chronic inflammatory diseases an increase in the plasma levels of oxprenolol has been observed. The plasma levels may also increase in the presence of severe hepatic insufficiency associated with a reduced metabolism.
Impaired renal function generally leads to an increase in the blood levels of oxprenolol, but the concentrations measured remain within – although at the upper limit of – the concentration range recorded in subjects with healthy kidneys. In addition, in patients with renal failure the apparent elimination half-life for unchanged, i.e. active, oxprenolol is comparable with the corresponding half-life values determined in subjects with no renal disease. Hence, there is no need to readjust the dosage in the presence of impaired renal function.
None stated.
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