Higher doses of clenbuterol may affect tissue excitability; such an effect may occur especially in conditions of hyperexcitability owing to use-dependent block of sodium channels. Interestingly, such a mechanism of action was recently proposed for the beneficial effect of clenbuterol in various seizure models of experimental epilepsy (Fischer et al., 2001

).
At the skeletal muscle level, sarcolemmal hyperexcitability leads to myotonia, a condition of muscle stiffness shared by various genetic muscle diseases (Cannon, 2001

; Moxley, 2000

; Meola, 2002

).
On the basis of our results, it would be important to verify the therapeutic potential of clenbuterol in the myotonic syndromes. In particular, because of the possibility of combining antimyotonic activity with its well known anabolic action, clenbuterol might be remarkably indicated in the treatment of myotonic dystrophy, the most common hereditary disease of skeletal muscle, characterized by muscle wasting together with permanent or fluctuans myotonia (Meola, 2002

).
On the other hand, because sodium channel block may accentuate paralysis, clenbuterol should not be administrated to patients with HPP, whereas other

2-agonists, such as salbutamol, have proven to be beneficial in those patients, most probably because

2-adrenoceptor stimulation activates the Na,K-ATPase and consequently hyperpolarizes the muscle fiber (Wang and Clausen, 1976

; Clausen et al., 1993

; Hanna et al., 1998

).