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甲状旁腺激素对尿液酸化的影响。

Effects of parathyroid hormone on urinary acidification.

作者信息

Bichara M, Mercier O, Paillard M, Leviel F

出版信息

Am J Physiol. 1986 Sep;251(3 Pt 2):F444-53. doi: 10.1152/ajprenal.1986.251.3.F444.

Abstract

Recollection micropuncture experiments were carried out in plasma-replete euvolemic thyroparathyroidectomized rats to examine the effects of a purified bovine parathyroid hormone (PTH) infusion on urinary acidification. After a 60-min equilibration period, PTH administration had the following effects: reabsorption in the proximal convoluted tubule was inhibited 13% for total CO2, 31% for chloride, and 28% for water; early distal delivery, however, remained unchanged for bicarbonate, chloride, and water principally as a result of stimulation of bicarbonate and chloride absorption in Henle's loop; the urinary bicarbonate and chloride excretion rates did not vary significantly, but the urinary pH decreased from 6.78 +/- 0.11 to 6.39 +/- 0.07 and titratable acid and ammonium excretion increased from 63 +/- 18 to 405 +/- 45 and from 422 +/- 30 to 647 +/- 44 nmol X min-1 X g kidney wt-1, respectively. In another group of rats, the bicarbonate urinary excretion rate increased more than twofold during the first 60 min of PTH infusion and then returned to control levels as was observed in the other groups; the transient increase in bicarbonaturia was attributable to a PTH-induced transient augmentation in glomerular filtration rate and bicarbonate filtered load. Finally, no change was noted in micropuncture or whole-kidney data in time-control rats. We conclude that PTH only transiently enhances the bicarbonate filtered load and urinary excretion rate during the first 60 min of administration secondary to an early hemodynamic action but that the steady effect is to stimulate urinary acidification and net acid excretion, which could generate metabolic alkalosis; and that the inhibition of the proximal bicarbonate and chloride reabsorption induced by PTH is counterbalanced by stimulation of reabsorption in Henle's loop.

摘要

在血浆充足、血容量正常的甲状腺甲状旁腺切除大鼠中进行了回收微穿刺实验,以研究纯化的牛甲状旁腺激素(PTH)输注对尿液酸化的影响。在60分钟的平衡期后,给予PTH产生了以下影响:近端曲管中二氧化碳总重吸收被抑制13%,氯化物重吸收被抑制31%,水重吸收被抑制28%;然而,早期远端输送的碳酸氢盐、氯化物和水基本保持不变,这主要是由于亨利袢中碳酸氢盐和氯化物吸收受到刺激;尿液中碳酸氢盐和氯化物排泄率没有显著变化,但尿液pH从6.78±0.11降至6.39±0.07,可滴定酸和铵排泄分别从63±18增至405±45和从422±30增至647±44 nmol·min⁻¹·g肾重⁻¹。在另一组大鼠中,PTH输注的前60分钟内碳酸氢盐尿排泄率增加了两倍多,然后如其他组所观察到的那样恢复到对照水平;碳酸氢盐尿的短暂增加归因于PTH诱导的肾小球滤过率和滤过的碳酸氢盐负荷的短暂增加。最后,时间对照大鼠的微穿刺或全肾数据未发现变化。我们得出结论,PTH在给药的前60分钟内仅通过早期血流动力学作用短暂增强滤过的碳酸氢盐负荷和尿排泄率,但稳定作用是刺激尿液酸化和净酸排泄,这可能导致代谢性碱中毒;并且PTH诱导的近端碳酸氢盐和氯化物重吸收的抑制被亨利袢中重吸收的刺激所抵消。

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