IntroductionIt is now well documented that DL propranolol produces a decrease in plasma concentrations of L-triiodothyronine (T 3 ) and a rise in serum reverse T 3 (rT 3 ) in euthyroid, hyperthyroid and hypothyroid subjects on thyroxine (T 4 ) supplements (Harrower, Fyffe, Horn and Strong 1977; Lumholtz, Siersbaek-Nielsen, Faber, Kirkegaard and Frits 1978;Jung, Shetty and James 1980). DL propranolol inhibits T 4 deiodination to T 3 at peripheral sites by a reduction of the T 3 production rate, the clearance of T 3 remaining unaltered (Lumholtz et al. 1978). The mechanism by which propranolol exerts this effect is unclear and may not be due solely to its (3-receptor blocking activity for L propranolol, which has no j3 blocking action but is a potent membrane stabiliser, and also reduces serum T 3 levels in hypothyroid subjects receiving T 4 replacement (Jones, Jones and Birtwell 1980).