The major adverse effects of j-receptor agonists occur as a result of excessive activation of b receptors: tremor, to which tolerance develops and which can be minimized by starting oral therapy with a low dose of drug and progressively increasing the dose as tolerance to the tremor develops; feelings of restlessness, apprehension, and anxiety, which may limit therapy; and tachycardia, primarily via j1 receptors but also possibly via cardiac j2 receptors, or to reflex effects that stem from j2 receptor—mediated peripheral vasodilation. During a severe asthma attack, heart rate actually may decrease during therapy with a j agonist, presumably because of improvement in pulmonary function with consequent reduction in endogenous cardiac sympathetic stimulation. In patients without cardiac disease, j agonists rarely cause significant arrhythmias or myocardial ischemia; however, patients with underlying coronary artery disease or preexisting arrhythmias are at greater risk. The risk of adverse cardiovascular effects is increased in patients receiving MAO inhibitors; 2 weeks should elapse between use of MAO inhibitors and administration of j2 agonists or other sympathomimetics. Severe pulmonary edema has been reported in women receiving ritodrine or terbutaline for premature labor.
Epidemiologic studies suggest a connection between prolonged use of j receptor agonists and death or near-death from asthma, raising questions about the role of j agonists in the treatment of chronic asthma. Tolerance to the pulmonary effects of these drugs is not a major clinical problem for the majority of asthmatics. Regular use of j2-selective agonists may cause increased bronchial hyperreactivity and deterioration in disease control; whether this potential adverse association may be more unfavorable for long-acting j agonists or excess doses is not yet known. For patients requiring regular use of j agonists over prolonged periods, strong consideration should be given to additional or alternative therapy (e.g., inhaled glucocorticoids). In some diabetic patients, j agonists may worsen hyperglycemia, and higher doses of insulin may be required. All these adverse effects are far less likely with inhalation therapy than with parenteral or oral therapy.
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