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肾小管周液黏度通过一氧化氮释放调节近端小管中的氢离子通量。

Peritubular fluid viscosity modulates H+ flux in proximal tubules through NO release.

作者信息

Díaz-Sylvester P, Mac Laughlin M, Amorena C

机构信息

Instituto de Investigaciones Cardiológicas-Consejo Nacional de Investigaciones Científicas y Técnicas, 1122 Buenos Aires, Argentina.

出版信息

Am J Physiol Renal Physiol. 2001 Feb;280(2):F239-43. doi: 10.1152/ajprenal.2001.280.2.F239.

DOI:10.1152/ajprenal.2001.280.2.F239
PMID:11208599
Abstract

We evaluated the effects of increasing the viscosity (eta) in peritubular capillary perfusates (PCP; 20 mM HNaPO4--Ringer, pH 7.4) on proximal convoluted tubule (PCT) acidification. Micropuncture experiments were performed with simultaneous luminal and peritubular perfusion. Changes in pH of a 20 mM HNaPO4--Ringer (pH 7.4 at t = 0) droplet placed in PCT lumen were measured with H+-sensitive microelectrodes. By adding neutral dextran (molecular wt 300,000-400,000) to the PCP, eta was increased. The effect of 10(-5) M ATP added to normal-eta PCP was evaluated. High eta increased H+ flux (85 and 97% when eta was increased 20 and 30%, respectively, above the control value). This increase was abolished by adding the nitric oxide antagonist N(omega)-nitro-L-arginine (L-NNA; 10(-4) M) or the purinoreceptor antagonists suramin (10(-4) M) and reactive blue 2 (3 x 10(-5) M). Addition of 5 x 10(-3) M L-arginine to the peritubular perfusate overcame the inhibitory effect of L-NNA on high-eta-induced increase in H+ flux. ATP increased H+ flux (80%), and this effect was blocked by L-NNA. These results suggest that changes in eta can modulate proximal H+ flux, at least in part, through ATP-dependent nitric oxide release from the endothelial cells of the peritubular capillaries.

摘要

我们评估了增加肾小管周围毛细血管灌流液(PCP;20 mM 磷酸氢二钠 - 林格液,pH 7.4)的黏度(η)对近端曲管(PCT)酸化的影响。采用管腔和肾小管周围同时灌流的方法进行微穿刺实验。用氢离子敏感微电极测量置于PCT管腔内的20 mM磷酸氢二钠 - 林格液(t = 0时pH 7.4)液滴的pH变化。通过向PCP中添加中性葡聚糖(分子量300,000 - 400,000)来增加η。评估了向正常η的PCP中添加10⁻⁵ M ATP的效果。高η增加了氢离子通量(当η分别比对照值增加20%和30%时,氢离子通量分别增加85%和97%)。添加一氧化氮拮抗剂N(ω)-硝基-L-精氨酸(L-NNA;10⁻⁴ M)或嘌呤受体拮抗剂苏拉明(10⁻⁴ M)和活性蓝2(3×10⁻⁵ M)可消除这种增加。向肾小管周围灌流液中添加5×10⁻³ M L-精氨酸可克服L-NNA对高η诱导的氢离子通量增加的抑制作用。ATP增加了氢离子通量(80%),且这种作用被L-NNA阻断。这些结果表明,η的变化至少部分地可通过肾小管周围毛细血管内皮细胞依赖ATP释放一氧化氮来调节近端氢离子通量。

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