Enhanced HCO3 secretion by distal tubule contributes to NaCl-induced correction of chronic alkalosis.

Enhanced HCO3 secretion by distal tubule contributes to NaCl-induced correction of chronic alkalosis.
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远端小管增强的 HCO3 分泌有助于 NaCl 诱导的慢性碱中毒的纠正。

DOI:
10.1152/ajprenal.1993.264.5.f899
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发表时间:
1993
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
G. Dolson
G. Dolson
中科院分区:
--
文献类型:
--
作者:
D. Wesson;G. Dolson

文献摘要

被引文献

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自由流动微穿刺研究表明,抑制净HCO 3重吸收在表面远端小管的大鼠进行纠正慢性代谢性水肿诱导NaCl输液。本研究使用大鼠远端小管的体内微灌注来研究所描述的净HCO 3重吸收的减少是否是由于管腔H+分泌减少或HCO 3分泌增加。无论灌注液最初是否不含Cl,纠正性肾积水的动物在该肾单位段的HCO 3分泌量均高于维持性肾积水的动物(-27.6 vs. -16.6 pmol.mm-1.min-1,P < 0.01)或含40 mM Cl(-31.5 vs. -23.0 pmol.mm-1.min-1,P < 0.01); H+分泌在纠正性和维持性肥大的动物之间没有差异。无水肿的动物(对照)对NaCl输注的反应显示H+或HCO 3分泌无差异。这些研究表明,增强HCO 3分泌介导的抑郁症净HCO 3重吸收观察到在远端小管的大鼠进行NaCl诱导的纠正慢性代谢紊乱。
Free-flow micropuncture studies show depressed net HCO3 reabsorption in the surface distal tubule of rats undergoing correction of chronic metabolic alkalosis induced by NaCl infusion. The present studies used in vivo microperfusion of the rat distal tubule to investigate whether the described reduction in net HCO3 reabsorption was due to decreased luminal H+ secretion or to increased HCO3 secretion. Animals with correcting alkalosis had higher HCO3 secretion in this nephron segment than did animals with maintained alkalosis regardless of whether the perfusing solution was initially Cl free (-27.6 vs. -16.6 pmol.mm-1.min-1, P < 0.01) or contained 40 mM Cl (-31.5 vs. -23.0 pmol.mm-1.min-1, P < 0.01); H+ secretion was not different between animals with correcting and maintained alkalosis. Animals without alkalosis (control) demonstrated no differences in H+ or HCO3 secretion in response to NaCl infusion. These studies demonstrate that enhanced HCO3 secretion mediates the depressed net HCO3 reabsorption observed in the distal tubule of rats undergoing NaCl-induced correction of chronic metabolic alkalosis.