[神经垂体非肽及其类似物对大鼠肾脏镁排泄的影响]。

A V Kutina, T A Karavashkina, D V Holasava, Yu V Natochin
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引用次数: 0

摘要

研究了脊椎动物神经垂体非肽(加压素、催产素及其合成类似物)对大鼠尿镁排泄的影响。神经垂体激素及其类似物在刺激v2受体(0.0001 ~ 0.001 nmol/100 g BW)剂量下产生抗利尿作用,减少尿镁排泄。在高剂量激活V2-和va1受体(0.025-0.1 nmol/100g BW)时,缩宫素及其类似物(去氨基缩宫素(dAVT)、去氨基缩宫素(thr4)、去氨基缩宫素(harg8)、去胺单碳缩宫素)可促进镁离子和钠离子的排泄。在这些条件下,钠和镁离子的肾脏排泄增加有直接关系。在给予v1a受体拮抗剂后,dAVT诱导的镁排泄量增加减少了10倍。v2受体拮抗剂不影响davt诱导的尿潴留。结果表明,v受体参与了大鼠肾脏镁转运的调控。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Effects of neurohypophysial nonapeptides and their analogues on magnesium excretion by rat kidney].

Effects of neurohypophysial nonapeptides of vertebrates (vasopressin, vasotocin, and their synthetized analogues) on urinary magnesium excretion were studied in rats. Neurohypophysial hormones and their analogues at doses stimulating V2-receptors (0.0001-0.001 nmol/100 g BW) produced antidiuretic effect and reduced urinary magnesium excretion. At the higher doses activating V2- and V1a-receptors (0.025-0.1 nmol/100g BW), vasotocin and its analogues (deamino-vasotocin (dAVT), deamino-Thr4-vasotocin, deamino-hArg8-vasotocin, deaminomonocarbo-vasotocin) enhanced excretion of magnesium and sodium ions. Direct relation between increase in renal excretion of sodium and magnesium ions was found under these conditions. dAVT induced 10 times lesser increase in magnesium excretion after administration of a V1a-receptor antagonist. An antagonist of V2-receptors did not affect the dAVT-induced magniuresis. The obtained data suggest that V-receptors take part in regulation of magnesium transport in rat kidney.

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