Aveten Mechanism of Action

Pharmacology: Pharmacodynamics: Atenolol is a beta- adrenoceptor blocking drug that is beta1- selective (i.e. acts preferentially on beta1- adrenergic receptors in the heart). Selectivity decreases with increasing dose.
Atenolol is without intrinsic sympathomimetic and membrane stabilizing activities and as with other beta-adrenoceptor blocking drugs, has negative inotropic effects (and is therefore contraindicated in uncontrolled heart failure).
As with other beta-adrenoceptor blocking drugs, the mode of action of atenolol in the treatment of hypertension is unclear. It is probably the action of atenolol in reducing cardiac rate and contractility that makes it effective in eliminating or reducing the symptoms of patients with angina.
It is unlikely that any additional ancillary properties possessed by S (-) atenolol, in comparison with the racemic mixture, will give rise to different therapeutic effects.
Atenolol is effective and well tolerated in most ethnic populations although the response may be less in black patients.
Atenolol is compatible with diuretics, other antihypertensive agents and antianginal agents.
Early intervention with atenolol in acute myocardial infarction reduces infarct size and decreases morbidity and mortality. Fewer patients with a threatened infarction progress to frank infarction; the incidence of ventricular arrhythmias is decreased and marked pain relief may result in reduced need of opiate analgesics. Early mortality is decreased. Atenolol is an additional treatment to standard coronary care.
Pharmacokinetics: Absorption of atenolol following oral dosing is consistent but incomplete ( approximately 40-50%) with peak plasma concentrations occurring 2-4 hours after dosing. The atenolol blood levels are consistent and subject to little variability. There is no significant hepatic metabolism of atenolol and more than 90% of that absorbed reaches the systemic circulation unaltered. The plasma half-life is about 6 hours but this may rise in severe renal impairment since the kidney is the major route of administration. Atenolol penetrates tissues poorly due to its low lipid solubility and its concentration in brain tissue is low. Plasma protein binding is low (approximately 3%).