&bgr;-Adrenoceptor blocking drugs (&bgr;-blockers) have an established place in the management of patients with thyroid disease. Thyroid hormones, however, markedly alter hepatic, renal and cardiovascular function and thus may significantly influence drug disposition. In hyperthyroidism the clearance of propranolol following intravenous administration is increased by approximately 50%, an effect that may be attributed to the marked increase in liver blood flow that occurs in this condition. On the other hand, the increased clearance of propranolol during long term oral therapy is presumably due to increased hepatic drug metabolising enzyme activity. However, following single oral doses the clearance of propranolol has been reported both to be unchanged and increased in hyperthyroid patients. Both during single dose and long term therapy the elimination half-life of propranolol is unaltered, in part due to an increased apparent volume of distribution. The degree of plasma protein binding of propranolol appears to be slightly reduced in the hyperthyroid state.There is evidence to suggest that the clearance of metoprolol, which like propranolol undergoes extensive hepatic metabolism, is also increased in hyperthyroidism. In contrast, the oral clearance of renally excreted &bgr;-blockers such as sotalol and atenolol, and probably practolol also, is not altered in hyperthyroidism.In general, all &bgr;-blockers produce a similar degree of symptomatic response. Those with intrinsic sympathomimetic activity (e.g. oxprenolol) do not reduce heart rate to the same extent as propranolol. Recent studies have shown a significant relationship between plasma propranolol levels and the objective measures (reduction in exercise tachycardia, serum triiodothyronine concentration and weight change) but not the subjective measures of therapeutic response. Concentration-response relationships are also becoming apparent for other &bgr;-blockers such as metoprolol and nadolol. The 20-fold interindividual variation in propranolol plasma concentrations, which may be largely attributed to age and smoking habits, emphasises the need for individualisation of dosage. This may also explain the reported cases of thyroid crisis, particularly postoperatively in patients receiving a fixed dosage regimen. In the latter situation surgery may also markedly alter the handling of propranolol.The effect of hypothyroidism on the disposition of &bgr;-blockers has not been definitively studied. In hypothyroidism the elimination half-life of propranolol following a single oral dose may be prolonged although clearance is not affected. During long term therapy, preliminary evidence suggests that steady-state plasma propranolol levels are elevated. The clearance of practolol is reduced and its elimination half-life is prolonged compared with the hyperthyroid state.It is unlikely that the efficacy of newer &bgr;-blockers will exceed that of propranolol. However, in certain clinical situations a long acting or a cardioselective agent may be preferable. The influence of thyroid disorders on the kinetics and the concentration-response relationships of the newer agents will, however, require further study.