CONTROL OF PULSATILE AND TONIC PARATHYROID-HORMONE SECRETION BY IONIZED CALCIUM

To investigate the effect of changes in ionized calcium on instantaneo us PTH secretion, we examined seven young healthy volunteers by 1-min blood sampling under conditions of normo-, hypo-, and hypercalcemia. A fter a baseline period of 75 min, ambient ionized calcium was either i ncreased or decreased by 0.2 mmol/L for 105 min by clamped infusion of calcium gluconate or sodium citrate. The characteristics of PTH secre tion were analyzed by a deconvolution technique, accounting for subjec t-specific plasma PTH disappearance half-life, as measured during the first 15 min of calcium infusion (range, 2.04-2.93 min). The process r egularity of pulsatile PTH secretion was evaluated by an approximate e ntropy statistic. Under baseline conditions, 32% of total PTH secretio n was released in a pulsatile fashion, with a burst frequency of 6.9+/ -0.8 h(-1) and a PTH mass per burst of 2.6+/-0.9 pmol/L. The remaining 68% of total secretion was attributed to tonic hormone release. Durin g the initial 30 min of induced hypocalcemia, pulsatile secretion incr eased by 1140%, whereas tonic secretion did not change. The preferenti al increase in pulsatile PTH secretion was mediated by a combined rise in burst frequency and mass released per burst. During subsequent ste ady state hypocalcemia, the tonic secretion rate increased (255% of ba seline), whereas burst frequency and burst mass decreased (to 103% and 189% of the baseline values), restoring the baseline ratio of tonic t o pulsatile PTH secretion. The regularity of PTH release increased dur ing steady state hypocalcemia. During hypercalcemia, tonic secretion, burst mass, and burst frequency decreased by 75%, 82%, and 32%, respec tively, and remained constant throughout the clamp period. We conclude that acute hypocalcemia elicits an immediate pulsatile and a delayed tonic secretory response of the parathyroid gland with increased regul arity of PTH release. Acute hypercalcemia suppresses both the pulsatil e and the tonic component of PTH secretion.