Tremor and β2-adrenergic agents: Is it a real clinical problem?

Tremor is one of the most characteristic adverse effects following administration of β2-adrenergic agonists. It is reported by around 2–4% of patients with asthma taking a regular β2-adrenergic agonist and is induced by both short-acting and long-acting agents. Tremor associated with β2-adrenergic agonists is dose-related and may occur more commonly with oral dosing. The exact mechanism for tremor induction by β2-adrenergic agonists is still unknown, but there is some evidence that β2-adrenergic agonists act directly on muscle. An early explanation of the tremor was that β2-adrenoceptor stimulation shortens the active state of skeletal muscle, which leads to incomplete fusion and reduced tension of tetanic contractions. More recently, tremor has been correlated closely with hypokalaemia. A possible diverse impact of different modes of administration of β2-adrenergic agonists on tremorogenic responses has been suggested but solid evidence is still lacking. In any case, the desensitization of β2-adrenoceptors that occurs during the first few days of regular use of a β2-adrenergic agonist accounts for the commonly observed resolution of tremor after the first few doses. Therefore, tremor is not a really important adverse effect in patients under regular treatment with a β2-adrenergic agonist.