Airways of asthma patients can become hyperresponsive to airway spasmogens following regular use of isoprenaline or β€ 2 -selective sympathomimetics. Hyperreactivity that results from acute exposure of animals to these drugs is pre-empted by vagal section (a procedure which does not influence spasmolytic efficacy of sympathomimetics), is not diminished by antagonism of β€ 2 -adrenoceptors and is not associated with loss of responsivity of β€ 2 -adrenoceptors in the airways. Since activation, modulation, or blockade of β€ 2 -adrenoceptors does not determine this form of hyperreactivity, the possibility that distomers may induce hyperreactivity must be considered. Ocular and vascular responses to distomers of sympathomimetics have long been recognised and, more recently, comparable observations have been made for the airways. Thus, reactivity of guinea-pig airways to spasmogens was increased following exposure to Sisoprenaline, S-salbutamol, or S-terbutaline and exposure to S-isoprenaline or Ssalbutamol can intensify symptoms in asthmatics. Regular exposure to the racemate, especially during or following an allergic reaction, predisposes to expression of hyperreactivity, which is nullified, acutely, by the eutomer. These observations imply that biological effects of sympathomimetic distomers may contribute to morbidity and mortality in asthma patients.