Prostaglandin-dependent polyuria in hypercalcemia.
Prostaglandin-dependent polyuria in hypercalcemia.
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高钙血症时前列腺素依赖性多尿。
DOI：
10.1152/ajprenal.1981.241.3.f224
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
M. Kirschenbaum
中科院分区：
文献类型：
--
作者：
E. Serros;M. Kirschenbaum
本实验研究了前列腺素生物合成在1，25-二羟基胆钙化醇诱导的高钙血症大鼠尿流率增加中的作用。在第一组中，接受维生素D代谢物的大鼠出现高钙血症、多尿和尿前列腺素E排泄增加。吲哚美辛导致尿前列腺素E排泄下降。第二组是液体限制，以确定是否增加口渴可能是多尿的病因机制。这导致尿流率轻微下降，尽管体重下降，尿液和血浆渗透压升高。在最后一组中，前列腺素抑制恢复了高钙肾的加压素敏感性。因此，高钙大鼠给予1，25-二羟基胆钙化醇后出现的多尿与尿前列腺素E排泄增加有关，可通过抑制前列腺素合成逆转。此外，这种多尿可以独立于口渴机制发生。最后，有证据表明，高钙肾的加压素抵抗可以通过前列腺素抑制来逆转。
The present experiments examined the role of prostaglandin biosynthesis in the increase in urine flow rate seen in rats with hypercalcemia induced by the administration of 1,25-dihydroxycholecalciferol. In a first group, rats receiving the vitamin D metabolite developed hypercalcemia, polyuria, and increased urine prostaglandin E excretion. Indomethacin resulted in a fall in urine prostaglandin E excretion. A second group was fluid restricted to ascertain whether increased thirst could be an etiologic mechanism of the polyuria. This resulted in a trivial fall in urine flow rate despite a fall in body weight and a rise in both urine and plasma osmolality. In a final group, prostaglandin inhibition restored the vasopressin sensitivity of the hypercalcemic kidney. Accordingly, the polyuria seen in hypercalcemic rats after the administration of 1,25-dihydroxycholecalciferol is associated with an increase in urine prostaglandin E excretion and can be reversed by inhibition of prostaglandin synthesis. In addition, this polyuria can occur independent of the thirst mechanism. Finally, there is evidence that the vasopressin resistance of the hypercalcemic kidney could be reversed by prostaglandin inhibition.