Summary1. AQ 110 is a 3-adrenoceptor agonist which, like isoprenaline and salbutamol, acts directly on the receptors. 2 Compared with isoprenaline, AQ 110 has relatively stronger actions on bronchial and vascular smooth muscle (P2-adrenoceptors) than stimulant effects on heart muscle (ft1-adrenoceptors). The fl2-selectivity of AQ 110 is, however, much less than that of salbutamol, mainly due to the weak cardiac actions of the latter.3. At doses which were equipotent in decreasing the bronchoconstrictor effect produced by a standard dose of 5-hydroxytryptamine, AQ 110 had marginally less hypotensive action than salbutamol and considerably less than isoprenaline. 4. Although AQ 110, unlike salbutamol, possesses a catechol group it was found not to be a substrate for catechol-O-methyl transferase and this is considered to account for its significantly prolonged action, compared with isoprenaline, in vivo.

1. The time-course of the rise in plasma renin activity (PRA) in response to an 2. The ability of racemic propranolol to inhibit this rise was confirmed. 3. This inhibition is shown to be due to antagonism of beta-adrenergic receptors rather than to the membrane-stabilizing properties of racemic propranolol.

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