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慢性碱中毒时大鼠远端肾小管增强的双向HCO3转运

Augmented bidirectional HCO3 transport by rat distal tubules in chronic alkalosis.

作者信息

Wesson D E, Dolson G M

机构信息

Veterans Affairs Medical Center, Baylor College of Medicine, Houston, Texas 77030.

出版信息

Am J Physiol. 1991 Aug;261(2 Pt 2):F308-17. doi: 10.1152/ajprenal.1991.261.2.F308.

DOI:10.1152/ajprenal.1991.261.2.F308
PMID:1877653
Abstract

Free-flow micropuncture studies show both augmented net HCO3 reabsorption in the distal tubule of rats with chronic metabolic alkalosis and higher HCO3 delivery to this nephron segment. The present studies in rats used in vivo microperfusion of surface distal tubules to investigate whether the augmented net reabsorption 1) was due to decreased HCO3 secretion and/or to increased proton secretion or 2) depended on the higher HCO3 delivery to the distal tubule. Artificial perfusates were designed to simulate in situ deliveries of HCO3 to the distal tubules of both alkalotic and control animals and to represent extremes of in situ Cl deliveries. Rather than being decreased, both measured and calculated HCO3 secretion were higher in the alkalotic animals for each perfusate used. Similarly, calculated proton secretion (difference between net HCO3 reabsorption and calculated HCO3 secretion) was higher for the alkalotic animals using each HCO3-containing perfusate. Augmented net HCO3 reabsorption by alkalotic animals was more clearly demonstrated using higher HCO3 deliveries and Cl-free perfusates. These studies demonstrate that both the reabsorptive and secretory components of net HCO3 transport are increased in the distal tubule of animals with chronic metabolic alkalosis.

摘要

自由流动微穿刺研究表明,慢性代谢性碱中毒大鼠的远端小管中,净HCO3重吸收增加,且该肾单位节段的HCO3输送量更高。本研究在大鼠体内对表面远端小管进行微灌注,以探究净重吸收增加是1)由于HCO3分泌减少和/或质子分泌增加,还是2)取决于远端小管中更高的HCO3输送量。人工灌注液的设计旨在模拟向碱中毒和对照动物的远端小管原位输送HCO3,并代表原位Cl输送的极端情况。对于所使用的每种灌注液,碱中毒动物中实测和计算得出的HCO3分泌均高于正常,而非降低。同样,对于使用每种含HCO3灌注液的碱中毒动物,计算得出的质子分泌(净HCO3重吸收与计算得出的HCO3分泌之间的差值)也更高。使用更高的HCO3输送量和无Cl灌注液时,碱中毒动物的净HCO3重吸收增加更为明显。这些研究表明,慢性代谢性碱中毒动物的远端小管中,净HCO3转运的重吸收和分泌成分均增加。

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