Dudczak R, Waldhäusl W K, Bratusch-Marrain P
J Clin Endocrinol Metab. 1983 Mar;56(3):603-7. doi: 10.1210/jcem-56-3-603.
To determine the impact of induced hypo- and hypercalcemia on TRH (400 micrograms)-stimulated TSH and PRL release, healthy subjects (n = 11) were infused with 5% glucose in water (n = 11), disodium EDTA (n = 11), or calcium gluconate (n = 7). TRH was given as an iv bolus 60 min (5% glucose and EDTA) and 120 min (calcium) after initiation of the respective infusion. Basal plasma concentrations of TSH remained unchanged during induced hypo- and hypercalcemia, whereas those of PRL fell during the latter (P less than 0.05). The mean sum of increments (0-90 min) in PRL and TSH was considerably greater during hypocalcemia than during hypercalcemia (PRL, P less than 0.002; TSH, P less than 0.005). The increments in the plasma hormone concentration above basal after iv TRH were increased compared to those in normocalcemia (PRL, 98.4 +/- 37.9 ng/ml; TSH, 38.9 +/- 11.8 microU/ml) during hypocalcemia [PRL, 128 +/- 47.8 ng/ml (P less than 0.002); TSH, 46.7 +/- 12.8 microU/ml; (P less than 0.005)], but were impaired during hypercalcemia [PRL, 70.1 +/- 27 ng/ml (P less than 0.002); TSH, 28.9 +/- 8.5 microU/ml (P less than 0.025)]. The mean sum of increments in PRL was related to concentrations of both serum calcium (r = -0.59; P less than 0.01) and PTH (r = 0.51; P less than 0.05). A relation was also seen between the incremental responses of TSH and serum calcium (r = -0.52; P less than 0.05), PTH (r = 0.55; P less than 0.01), and phosphorus (r = -0.55; P less than 0.01). We conclude that in healthy man, TRH-mediated release of both PRL and TSH are inversely related to serum calcium concentrations in such a manner that hormone secretion is enhanced by acute hypocalcemia, but blunted by hypercalcemia.
为了确定低钙血症和高钙血症对促甲状腺激素释放激素（TRH，400微克）刺激的促甲状腺激素（TSH）和催乳素（PRL）释放的影响，将健康受试者（n = 11）分别输注5%葡萄糖水溶液（n = 11）、乙二胺四乙酸二钠（n = 11）或葡萄糖酸钙（n = 7）。在开始相应输注后60分钟（5%葡萄糖和乙二胺四乙酸）和120分钟（葡萄糖酸钙）静脉推注TRH。在诱导的低钙血症和高钙血症期间，基础血浆TSH浓度保持不变，而PRL浓度在高钙血症期间下降（P < 0.05）。低钙血症期间PRL和TSH的平均增量总和（0 - 90分钟）明显大于高钙血症期间（PRL，P < 0.002；TSH，P < 0.005）。与正常血钙水平相比，静脉注射TRH后血浆激素浓度高于基础值的增量在低钙血症期间增加[PRL，98.4 ± 37.9纳克/毫升；TSH，38.9 ± 11.8微国际单位/毫升] [PRL，128 ± 47.8纳克/毫升（P < 0.002）；TSH，46.7 ± 12.8微国际单位/毫升；（P < 0.005）]，但在高钙血症期间受损[PRL，70.1 ± 27纳克/毫升（P < 0.002）；TSH，28.9 ± 8.5微国际单位/毫升（P < 0.025）]。PRL增量的平均总和与血清钙浓度（r = -0.59；P < 0.01）和甲状旁腺激素（PTH）浓度（r = 0.51；P < 0.05）均相关。TSH的增量反应与血清钙（r = -0.52；P < 0.05）、PTH（r = 0.55；P < 0.01）和磷（r = -0.55；P < 0.01）之间也存在相关性。我们得出结论，在健康男性中，TRH介导的PRL和TSH释放与血清钙浓度呈负相关，即急性低钙血症可增强激素分泌，而高钙血症则使其减弱。
