Faculty Bibliography

Nine uraemic patients not being treated by dialysis received intravenous propranolol 1 microgram/kg/min for 85 minutes after a priming dose of 1 mg. Fifteen days later, six of them received intravenous metoprolol 1.2 microgram/kg/min after a priming dose of 1.2 mg. Plasma concentrations of parathyroid hormone (PTH) and calcitonin fell significantly after propranolol but not after metoprolol, whereas no change in plasma concentrations of ionised calcium and phosphate occurred with either drug. Heart rate fell similarly with both drugs. The fact that propranolol acutely suppressed PTH and calcitonin secretion in uraemic patients indicates that further studies are warranted to assess the long-term effects of the drug on the secretion of these hormones and on renal osteodystrophy. The contrast between the responses to propranolol and metoprolol supports the concept that PTH and calcitonin secretion is modulated through specific beta 2-receptors.

Calcitonin treatment of animals injected with DS sarcoma cells inhibits partially both the take of the tumor and the formation of metastasis. This phenomenon is discussed in relation to the pharmacological and immunological properties of the hormone.

In order to determine the effect of beta-blocking agents on secretions of parathyroid hormone and calcitonin, 9 patients with renal failure were given single doses of propranolol (a blocker of the beta 1 and beta 2 receptors) or an equivalent amount of metoprolol (a beta 1 selective agent). Propranolol causes a decrease of plasma parathyroid hormone (p less than 0.02) as well as of calcitonin (p less than 0.05) whereas metoprolol has no effect on the plasma levels of these hormones. These findings suggest that parathyroid tissue and thyroid C cells have receptors that are exclusively of the beta 2 type which are modulating the secretion of parathyroid hormone and calcitonin.

Nine uraemic patients not yet on dialysis received IV 1 microgram/kg/min of propranolol for 85 min after a priming dose of 1 mg. Fifteen days later six of them received IV 1.2 microgram/kg/min of metoprolol after a priming dose of 1.2 mg. Plasma concentrations of PTH and calcitonin decreased significantly with propranolol but not with metoprolol. No change was observed with either drug as regards plasma concentration of total and ionised Ca and PO4. Heart rate was decreased similarly with both drugs. We conclude that (i) propranolol acutely suppresses PTH and Calcitonin secretion in uraemic patients. This warrants further studies to assess its long term effects on the secretion of these hormones and on renal osteodystrophy; (ii) the contrast between the significant effect of propranolol and the lack of effect with metoprolol supports the concept that PTH and CT secretion are moderated through specific beta 2 receptors.