Beta-adrenergic system and parathyroid hormone secretion: Effect of beta-adrenergic blocking upon PTH secretion in uremic patients and in patients with acute myocardial infarction

Calcium, calcitriol and phosphorus are the most important factors regulating PTH secretion. There is evidence of beta-adrenergic influence in parathyroid cells function vitro studies have shown the existence of beta-adrenergic receptors and adenyl-cyclase system in parathyroid cells and some of those studies have verified changes in PTH levels after administration of beta-adrenergic blockers and beta-adrenergic agonistc. The effect of beta-adrenergic blockers on the PTH secretion in uremic patients has not been studied. We have analyzed the PTH/calcium curve in nine patients with CRF, undergoing HD treatment, before and after 30 days on oral propranolol. We also studied the effect of intravenous propranolol on PTH levels in sate with increased levels of catecholamines, such as acute myocardial infarction. In patients undergoing HD, the serum levels of propranolol were 1,93 +/- mcg/ml after propranolol intake. Mean arterial pressure and heart rate decreased significantly. Values of basal PTH after propranolol (588 +/- 111 pg/ml) were less than basal values before it (658 +/- 123 pg/ml), although the difference was not significant. Basal blood values of ionic calcium, total calcium, albumin, bicarbonate, phosphorus, magnesium, hematocrit and 1,25(OH)2D3 were similar before ad during treatment. We did nor observe significant differences in the PTH/calcium curve that would indicate changes in the functional secretory capacity, parathyroid suppresibility or sensitivity of parathyroid cell to calcium. Thus, values of maximum PTH (1614 +/- 240 vs 1549 +/- 340 pg/ml), the basal PTH/maximum PTH ratio (39,64 +/- 3,62 vs 41,16 +/- 4,3 %) minimum PTH (254 +/- 76 vs 263 +/- 79 pg/ml), the minimum PTH/maximum PTH ratio (14,32 +/- 3 vs 16,05 +/- 2,6 %), set point (4,59 +/- 0, 14 vs 4,64 +/- 0, 1 mg/dl) and slope (-1,33 +/- 0,19 vs -1,54 +/- 0,35) were similar before and during propranolol therapy. In patients with acute myocardial infarction we observed increased basal levels of serum PTH (72,5 +/- 11,1 pg/ml) with normal values of ionic calcium. After 15 and 30 minutes of intravenous administration of propranolol, PTH levels decrease, although not significantly (54 +/- 7 and 60,2 +/- 7,7), and with no changes in levels of ionic calcium, phosphorus or magnesium. The absence of beta-adrenergic blocking effect on basal levels of PTH and on the PTH-calcium curve suggests that in uremic patients undergoing HD treatment, the PTH secretion is not under the tonic influence of adrenergic system and it does not take part in the response of PTH to acute hypo- and hypercalcemia. On the other hand, in situations with increased levels of catecholamines, such as acute myocardial infarction, there is an increase of PTH secretion, that is not modified by propranolol administration.