3522 Atenolol Atenolol is a so-called beta1-selective (or 'cardioselective') drug. That means that it exerts greater blocking activity on myocardial beta1-receptors than on beta2 ones in the lung. The beta2 receptors are responsible to keep the bronchial system open. If these receptors are blocked, bronchospasm with serious lack of oxygen in the body can result. However, due to its cardioselective properties, the risk of bronchospastic reactions if using atenolol is reduced compared to nonselective drugs as propranolol. Nonetheless, this reaction may also be encountered with atenolol, particularly with high doses. Extreme caution should be exerted if atenolol is given to asthma patients, who are particularly at risk; the dose should be as low as possible. If an asthma attack occurs, the inhalation of a beta2-mimetic antiasthmatic, such as hexoprenalin or salbutamol, will usually suppress the symptoms. Atenolol (trade name Tenormin) can be used to treat cardiovascular diseases such as hypertension, coronary heart disease, arrhythmias, and treatment of myocardial infarction after the acute event. Patients with compensated congestive heart failure may be treated with atenolol as a co medication (usually together with an ACE inhibitor, a diuretic and a digitalis-glycoside, if indicated). In patients with congestive heart failure, it reduces the need for and the consumption of oxygen of the heart muscle. It is very important to start with low doses, as atenolol reduces also the muscular power of the heart, which is an undesired effect in congestive heart failure. 29122-68-7 2249 C14H22N2O3 266.163040 White powder. 158-160°C 1.33E+004 mg/L (at 25°C) Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, the remainder being excreted unchanged in the feces. Like metoprolol, atenolol competes with sympathomimetic neurotransmitters such as catecholamines for binding at beta(1)-adrenergic receptors in the heart and vascular smooth muscle, inhibiting sympathetic stimulation. This results in a reduction in resting heart rate, cardiac output, systolic and diastolic blood pressure, and reflex orthostatic hypotension. Higher doses of atenolol also competitively block beta(2)-adrenergic responses in the bronchial and vascular smooth muscles. Hepatic (minimal) Route of Elimination: Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, the remainder being excreted unchanged in the feces. Unlike propranolol or metoprolol, but like nadolol, atenolol undergoes little or no metabolism by the liver, and the absorbed portion is eliminated primarily by renal excretion. Half Life: 6-7 hours LD50: 2000-3000 mg/kg(oral, mice). No indication of carcinogenicity to humans (not listed by IARC). For the management of hypertention and long-term management of patients with angina pectoris Symptoms of an atenolol overdose include a slow heart beat, shortness of breath, fainting, dizziness, weakness, confusion, nausea, and vomiting. 2009-07-30T17:58:38Z 2014-12-24T20:26:07Z Atenolol C13235 2904 Atenolol DB00335 true CC(C)NCC(O)COC1=CC=C(CC(O)=N)C=C1 C14H22N2O3 InChI=1/C14H22N2O3/c1-10(2)16-8-12(17)9-19-13-5-3-11(4-6-13)7-14(15)18/h3-6,10,12,16-17H,7-9H2,1-2H3,(H2,15,18) InChIKey=METKIMKYRPQLGS-UHFFFAOYNA-N 266.3361 266.16304258 Exogenous Solid 0.16 HMDB01924 CHEMBL24 2162 <p>Barrett, A.M., Carter, J., Hull, R., Le Count, D.J. and Squire, C.J.; U.S. Patent 3,663,607;<br /> May 16, 1972; assigned to Imperial Chemical Industries Limited, England.<br /> Barrett, A.M., Carter, J., Hull, R., Le Count, D.J. and Squire, C.J.; U.S. Patent 3,836,671;<br /> September 17, 1974; assigned to Imperial Chemical Industries Limited, England.</p>