Paradoxical vocal cord adduction in cystic fibrosis.

look at first glance as though ICI 118 551 has no effect on exercise-induced hyperkalaemia compared with placebo. However, the baseline potassium concentration was significantly lower in the ICI 118 551 group than in the placebo group, and this may explain the apparent lack of effect on exercise response. Furthermore, in that study atenolol had no effect on the exercise-induced potassium response, suggesting that ,13 receptors are not involved. Indeed, in our own study salbutamol had no effect on the exercise heart rate response, showing that PI3 blockade did not occur. It has also been shown that a low dose of nadolol (5 mg), which has a minimal P, blockade, exhibits marked P2 blockade as assessed by exercise-induced hyperkalaemia.3 Thus, the fact that in our study both salbutamol and propranolol significantly augmented the exercise-induced potassium response is in keeping with a P2 receptor mediator mechanism linked to the Na/KATPase pump. This hypothesis is further supported by the enhancement of exercise-induced hyperkalaemia by digitalis which directly inhibits the Na/K-ATPase pump.4 We therefore remain of the firm opinion that, in the presence of high adrenergic tone, salbutamol exhibits 12 antagonist activity as demonstrated by augmentation of exerciseinduced hyperkalaemia. This would be in keeping with the known pharmacological properties ofsalbutamol as a partial P2 agonist along with in vitro data showing salbutamol to antagonise the relaxant effect of isoprenaline in the presence of carbacholinduced bronchoconstriction.5 Whilst we agree that salbutamol is of great value in treating acute bronchospasm, it may be that a P2 agonist with greater intrinsic activity may be preferable in certain situations where airway tone is increased.