BETA-ADRENERGIC SYSTEM AND PARATHYROID-HO RMONE SECRETION - EFFECT OFBETA-ADRENERGIC BLOCKING UPON PTH SECRETION IN UREMIC PATIENTS AND INPATIENTS WITH ACUTE MYOCARDIAL-INFARCTION

Calcium, calcitriol and phosphorus are the most important factors regu lating PTH secretion. There is evidence of beta-adrenergic influence i n parathyroid cells function vitro studies have shown the existence of beta-adrenergic receptors and adenyl-cyclase system in parathyroid ce lls and some of those studies have verified changes in PTH levels afte r administration of beta-adrenergic blockers and beta-adrenergic agoni stc. The effect of beta-adrenergic blockers on the PTH secretion in ur emic patients has not been studied. We have analyzed the PTH/calcium c urve in nine patients with CRF, undergoing HD treatment, before and af ter 30 days on oral propranolol. We also studied the effect of intrave nous propranolol on PTH levels in sate with increased levels of catech olamines, such as acute myocardial infarction. In patients undergoing HD, the serum levels of propranolol were 1,93 +/- mcg/ml after propran olol intake. Mean arterial pressure and heart rate decreased significa ntly. Values of basal PTH after propranolol (588 +/- 111 pg/ml) were l ess than basal values before it (658 +/- 123 pg/ml), although the diff erence 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 observ e significant differences in the PTH/calcium curve that would indicate changes in the functional secretory capacity, parathyroid suppresibil ity or sensitivity of parathyroid cell to calcium. Thus, values of max imum PTH (1614 +/- 240 vs 1549 +/- 340 pg/ml), the basal PTH/maximum P TH ratio (39,64 +/- 3,62 vs 41,16 +/- 4,3 %) minimum PTH (254 +/- 76 v s 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) a nd slope (-1,33 +/- 0,19 vs -1,54 +/- 0,35) were similar before and du ring 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 intra venous administration of propranolol, PTH levels decrease, although no t significantly (54 +/- 7 and 60,2 +/- 7,7), and with no changes in le vels of ionic calcium, phosphorus or magnesium. The absence of beta-ad renergic blocking effect on basal levels of PTH and on the PTH-calcium curve suggests that in uremic patients undergoing HD treatment, the P TH 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 hyper calcemia. On the other hand, in situations with increased levels of ca techolamines, such as acute myocardial infarction, there is an increas e of PTH secretion, that is not modified by propranolol administration .