Humes H D, Simmons C F, Brenner B M
Am J Physiol. 1980 Sep;239(3):F244-9. doi: 10.1152/ajprenal.1980.239.3.F244.
Experiments were performed on 26 acutely thyroparathyroidectomized (TPTX) Sprague-Dawley rats undergoing maximum water diuresis to determine whether the rise in urinary osmolality (Uosmol) in response to a submaximal dose of antidiuretic hormone (ADH) is modified by exogenous administration of parathyroid hormone (PTH). During administration of a submaximal dose of PTH to 11 TPTX rats, the ADH-induced increase in Uosmol averaged 267 +/- 15 mosmol, or twice the average increment of 131 +/- 18 mosmol observed when the same dose of ADH was given prior to PTH infusion (P < 0.001). This difference could not be attributed to changes in endogenous ADH release, renal hemodynamics, or solute excretion, and was not observed in a second group of eight other water-diuretic TPTX rats given sham PTH infusion. A third group of seven water-diuretic TPTX rats were studied with verapamil, a compound known to antagonize calcium ion entry into cells. Pretreatment of these rats with intravenous verapamil abolished the PTH potentiation of the Uosmol response to ADH described above. We conclude, therefore, that PTH enhances the Uosmol response to ADH, perhaps via a mechanism requiring a PTH-mediated change in the cellular calcium concentration or content of cells important in the urinary concentrating process.
对26只正在进行最大水利尿的急性甲状旁腺甲状腺切除（TPTX）的Sprague-Dawley大鼠进行实验，以确定甲状旁腺激素（PTH）的外源性给药是否会改变抗利尿激素（ADH）亚最大剂量引起的尿渗透压（Uosmol）升高。在对11只TPTX大鼠给予亚最大剂量PTH的过程中，ADH诱导的Uosmol平均增加267±15 mosmol，是在PTH输注前给予相同剂量ADH时观察到的平均增加量131±18 mosmol的两倍（P<0.001）。这种差异不能归因于内源性ADH释放、肾血流动力学或溶质排泄的变化，并且在另一组接受假PTH输注的8只其他水利尿TPTX大鼠中未观察到。对第三组7只水利尿TPTX大鼠用维拉帕米进行研究，维拉帕米是一种已知可拮抗钙离子进入细胞的化合物。用静脉注射维拉帕米预处理这些大鼠消除了上述PTH对ADH引起的Uosmol反应的增强作用。因此，我们得出结论，PTH可能通过一种需要PTH介导的参与尿液浓缩过程的细胞钙浓度或细胞内钙含量变化的机制来增强对ADH的Uosmol反应。
