Berl T
Kidney Int. 1981 Jan;19(1):15-23. doi: 10.1038/ki.1981.3.
The role of cellular calcium uptake in the antidiuretic response to vasopressin was studied in anesthetized dogs undergoing water diuresis. In prostaglandin (PG) intact animals, an intrarenal infusion of verapamil caused only a modest blunting of the response to antidiuretic hormone (ADH), because the urinary osmolality (UOsm) achieved in the contralateral control kidney was 338 +/- 40 mOsm/kg H2O but was only 270 +/- 23 mOsm/kg H2O in the verapamil-infused kidney. The possibility was then studied that PG inhibit the action of ADH by impairing cellular calcium uptake. If so, verapamil would be expected to abolish the effect of PG inhibition to enhance the action of ADH. In eight PG-inhibited dogs, the control kidney's UOsm increased to a mean of 650 +/- 103 mOsm/kg H2O but only to 280 +/- 22 mOsm/kg H2O in the infused side. Thus, verapamil abolished the effect of PG inhibition to enhance the action of ADH. Likewise in five dogs a second chemically dissimilar inhibitor of calcium transport, proadifen, also abolished the effect of PG inhibitors as UOsm rose to 590 +/- 78 mOsm/kg H2O in the control kidney but only to 278 +/- 11 mOsm/kg H2O in the proadifen-infused kidney. Neither prior vasodilatation nor an increased solute excretion with mannitol of a degree observed with verapamil mimicked the effect of the calcium uptake blockers to inhibit the action of ADH. The present in vivo studies therefore demonstrate that the effect of PG inhibitors to enhance the hydroosmotic effect of vasopressin involve cellular calcium transport.
在进行水利尿的麻醉犬中，研究了细胞钙摄取在血管加压素抗利尿反应中的作用。在前列腺素（PG）完整的动物中，肾内输注维拉帕米仅使对抗利尿激素（ADH）的反应略有减弱，因为对侧对照肾达到的尿渗透压（UOsm）为338±40 mOsm/kg H₂O，而在输注维拉帕米的肾脏中仅为270±23 mOsm/kg H₂O。随后研究了PG是否通过损害细胞钙摄取来抑制ADH的作用。如果是这样，预计维拉帕米将消除PG抑制增强ADH作用的效应。在8只PG抑制的犬中，对照肾的UOsm平均增加到650±103 mOsm/kg H₂O，但在输注侧仅增加到280±22 mOsm/kg H₂O。因此，维拉帕米消除了PG抑制增强ADH作用的效应。同样，在5只犬中，另一种化学性质不同的钙转运抑制剂普罗地芬也消除了PG抑制剂的效应，因为对照肾的UOsm升至590±78 mOsm/kg H₂O，而在输注普罗地芬的肾脏中仅升至278±11 mOsm/kg H₂O。维拉帕米观察到的先前血管舒张或甘露醇引起的溶质排泄增加程度均未模拟钙摄取阻滞剂抑制ADH作用的效应。因此，目前的体内研究表明，PG抑制剂增强血管加压素水渗透效应的作用涉及细胞钙转运。
