Effect of oral propranolol on parathyroid hormone secretion in chronic renal failure

Parathyroid hormone secretion is stimulated by beta-adrenergic agents and this effect is blocked by propranolol. Acute infusion of propranolol in uraemic patients has been shown to inhibit secretion of parathyroid hormone, and a retrospective study has suggested that treatment with beta-blockers may protect against secondary hyperparathyroidism in haemodialysis patients. We report a prospective study designed to assess the long-term effects of oral propranolol on plasma parathyroid hormone concentrations in haemodialysis patients. The beta-adrenergic-blocking activity by the doses of propranolol given was significant as judged by the abolition of isoprenaline-induced rises in pulse rate. Plasma concentrations of immunoreactive parathyroid hormone fell during treatment, and this may indicate a direct effect of propranolol on beta-adrenergic receptors in parathyroid tissue. The degree of parathyroid gland suppression during acute propranolol infusion in uraemic patients was much greater than that observed in this study. The differences may be accounted for by the significant rise in plasma phosphate concentrations which also occurred during this study. In normal circumstances this would lower plasma ionised calcium concentrations, which would tend to stimulate parathyroid hormone secretion. Hence the low plasma concentrations of immunoreactive parathryoid hormone seen may underestimate the actual degree of parathryoid hormone suppression achieved by propranolol. There were, however, only small reductions in concentrations of immunoreactive parathyroid hormone after three months' treatment, and we doubt whether propranolol has a role in the treatment of established hyperparathyroid bone disease in chronic renal failure.