antagonists (also called beta blockers) are usedfor long-term
prevention of angina and are one of the main types of drugs used to treat
hypertension. Beta-adrenergic blockers in-clude:
Metoprolol and propranolol are absorbed almost
entirely from the GI tract, whereas less than one-half the dose of atenolol or
nadolol is absorbed. These beta-adrenergic blockers are distrib-uted widely.
Propranolol is highly protein-bound; the other beta-adrenergic blockers are
Propranolol and metoprolol are metabolized in the
liver, and their metabolites are excreted in urine. Atenolol and nadolol aren’t
me-tabolized and are excreted unchanged in urine and stool.
Beta-adrenergic blockers decrease blood pressure
and block beta-adrenergic receptor sites in the heart muscle and the conduction
system. This decreases the heart rate and reduces the force of the heart’s
contractions, resulting in a lower demand for oxygen.
Beta-adrenergic blockers are indicated for
long-term prevention of angina. In acute coronary syndrome, metoprolol may be
given ini-tially I.V., and then orally. Metoprolol may also be used for heart
Because of their ability to reduce blood pressure,
beta-adren-ergic blockers are also first-line therapy for treating
A number of drugs interact with beta-adrenergic
Antacids reduce absorption of beta-adrenergic blockers.
Nonsteroidal anti-inflammatory drugs (NSAIDs) can decrease the
hypotensive effects of beta-adrenergic blockers.
Cardiac glycosides and calcium channel blockers can have neg-ative
addictive effects on SA or AV node conduction when admin-istered with a
Diuretics or other hypotensive agents can potentiate the hy-potensive
effects of beta-adrenergic blockers.
Lidocaine toxicity may occur when lidocaine is taken with
The requirements for insulin and oral antidiabetics can be al-tered by
The ability of theophylline to produce bronchodilation is im-paired by
nonselective beta-adrenergic blockers. (See Adverse
re-actions to beta-adrenergic blockers.)