1. The metabolism of the beta-adrenergic blocking agent practolol has been studied in a variety of small animal species, using both ring- and acetyl-14C-labelled material. After oral dosing at 100 mg/kg, elimination of 14C in urine and expired air was monitored, and urinary metabolite patterns were examined by t.l.c. 2. Marmoset was unusual in extensively deacetylating practolol (c. 57% dose). Urinary elimination was low, with only 25% being recovered in 4 days; over 30% of urinary 14C was present as desacetyl practolol, whereas less than 50% was unchanged practolol. 3. Hamster was also atypical, in its extensive hydroxylation of practolol. Urine contained 60% dose; 11% of urinary radioactivity was present as 3-hydroxypractolol, much of the polar material present (48%) appeared to be a conjugate of this, and only 35% was present as practolol. 4. For the other species studied (rat, mouse, guinea-pig and rabbit, metabolism was more limited. Deacetylation was typically about 5%, but was somewhat higher in the mouse (8--14%). Urine was the major route of elimination and practolol represented 50--90% of urinary radioactivity. 5. Despite extensive toxicity studies, both in species which metabolize practolol similarly to man and in species such as the hamster and marmoset which metabolize practolol extensively, no animal model has been found for the human adverse reactions.