[大鼠缺氧和低碳酸血症时甲状旁腺激素的磷酸化作用]。

Y Mimura
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引用次数: 0

摘要

本研究探讨急性缺氧或低碳酸血症对去甲状旁腺大鼠肾磷排泄的影响。缺氧通常伴有缺氧过度通气引起的继发性低碳酸血症。呼吸性碱中毒被描述为削弱甲状旁腺激素(PTH)的磷酸化作用。在本研究中,为了了解无低碳酸血症情况下缺氧对肾磷排泄的影响,我们对大鼠进行机械通气,并控制动脉PCO2水平。根据动脉血PO2和PCO2水平将大鼠分为3组:1)低氧正氧组;2)正氧组;3)常氧低碳酸组。通过10%氧气换气实现缺氧,通过25-30%氧气过度换气实现低碳酸血症。在低氧组(n = 7), PTH输注显著增加磷酸盐(FEPi)分数排泄,从4.1 +/- 0.9(平均+/- SE)增加到37.7 +/- 2.6%;在常氧组(n = 8),从1.4 +/- 0.3增加到27.4 +/- 2.5%;在低氧组(n = 10),从1.5 +/- 0.4增加到19.5 +/- 1.2%。低氧时PTH输注后FEPi (δ FEPi)的变化(33.6 +/- 2.1%)显著大于常氧时(26.1 +/- 2.4%,p < 0.05)。与此相反,低碳酸降低了PTH的磷酸化反应(18.0 +/- 1.1% δ FEPi, p < 0.05)。PTH输注后三组尿腺苷3′,5′-环单磷酸腺苷(cAMP)均升高。为了检验缺氧时甲状旁腺激素磷酸化作用的增强和低碳酸血症时甲状旁腺激素磷酸化作用的减弱是否由于超出了cAMP的产生,三组均给予cAMP。与常氧组(n = 6, 24.1 +/- 1.0%)相比,低氧组(n = 6, 30.0 +/- 1.4%)出现了更多的磷尿(n = 6, 30.0 +/- 1.4%),低氧组(n = 7, 11.3 +/- 1.8%)出现了更少的磷尿(n = 6, 24.1 +/- 1.0%)。综上所述,急性缺氧可增强甲状旁腺激素的磷酸化作用,而急性低碳酸血症可减弱甲状旁腺激素的磷酸化作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Phosphaturic effect of PTH during hypoxia and hypocapnia in rats].

This study examined the effect of acute hypoxia or hypocapnia on renal phosphate excretion in thyroparathyroidectomized rats. Hypoxia is usually accompanied by a secondary hypocapnia due to hypoxic hyperventilation. Respiratory alkalosis has been described as blunting the phosphaturic effect of parathyroid hormone (PTH). In the present study, to know the effect of hypoxia on renal phosphate excretion in the absence of hypocapnia, the rats were ventilated mechanically, and arterial PCO2 levels were controlled. The rats were divided into three groups depending on the arterial PO2 and PCO2 levels: 1) hypoxic normocapnic group; 2) normoxic normocapnic group; 3) normoxic hypocapnic group. Hypoxia was achieved by ventilating with 10% oxygen, and hypocapnia by hyperventilating with 25-30% oxygen. PTH infusion significantly increased fractional excretion of phosphate (FEPi) from 4.1 +/- 0.9 (mean +/- SE) to 37.7 +/- 2.6% in the hypoxic group (n = 7), from 1.4 +/- 0.3 to 27.4 +/- 2.5% in the normoxic group (n = 8), and from 1.5 +/- 0.4 to 19.5 +/- 1.2% in the hypocapnic group (n = 10). The change of FEPi (delta FEPi) after PTH infusion during hypoxia was significantly greater (33.6 +/- 2.1%) than that during normoxia (26.1 +/- 2.4%, p < 0.05). In contrast to this, hypocapnia blunted the phosphaturic response to PTH (18.0 +/- 1.1% delta FEPi, p < 0.05). Urinary adenosine 3', 5'-cyclic monophosphate (cAMP) increased similarly after PTH infusion in all three groups. To test whether the enhanced phosphaturic effect of PTH during hypoxia and the blunted phosphaturic effect of PTH during hypocapnia are due to steps beyond the production of cAMP, cAMP was administered to the three groups. Cyclic AMP infusion displayed greater phosphaturia in the hypoxic group (n = 6, 30.0 +/- 1.4%) and less phosphaturia in the hypocapnic group (n = 7, 11.3 +/- 1.8%) as compared the the normoxic group (n = 6, 24.1 +/- 1.0%). In conclusion, acute hypoxia enhances the phosphaturic effect of PTH, whereas acute hypocapnia attenuates the phosphaturic effect of PTH.

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