FORMOTEROL ON AIRWAY SMOOTH-MUSCLE AND HUMAN LUNG MAST-CELLS - A COMPARISON WITH SALBUTAMOL AND SALMETEROL

Formoterol, like salbutamol and salmeterol, relaxed isolated preparati ons of guinea-pig trachea and human bronchus, and inhibited antigen-in duced mediator release from human lung fragments in a concentration-re lated fashion. In each case, these actions were mediated through beta( 2)-adrenoceptors, with formoterol being 50-120-fold more potent than s albutamol, and 2-27-fold more potent than salmeterol. The duration of action of formoterol was longer than that of salbutamol in all prepara tions, but was markedly shorter than that of salmeterol, whose actions persisted for many hours despite continuous or extensive washing of t he tissues. In conscious guinea-pigs, inhaled formoterol, salbutamol a nd salmeterol all caused dose-related inhibition of histamine-induced bronchoconstriction. Formoterol was again more potent (10-20-fold) tha n either salbutamol or salmeterol. However, while the actions of a thr eshold-effective dose of formoterol persisted for less than 3 h, somew hat longer than those of salbutamol(< 1.5 h), an equivalent dose of sa lmeterol was active for at least 6 h. Therefore, while formoterol is a potent beta(2)-adrenoceptor agonist in vitro and in vivo, and is cons istently longer-acting than salbutamol, its duration of action is mark edly shorter than that of salmeterol.