首页> 美国卫生研究院文献>The Journal of Clinical Investigation >Ion transport in proximal colon of the rat. Sodium depletion stimulates neutral sodium chloride absorption.
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Ion transport in proximal colon of the rat. Sodium depletion stimulates neutral sodium chloride absorption.

机译:大鼠近端结肠中的离子运输。钠的消耗会刺激中性氯化钠的吸收。

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摘要

The model of sodium and chloride transport proposed for the colon is based on studies performed in the distal segment and tacitly assumes that ion transport is similar throughout the colon. In rat distal colon, neutral sodium-chloride absorption accounts for the major fraction of overall sodium absorption and aldosterone stimulates electrogenic, amiloride-sensitive sodium absorption. Since we have demonstrated qualitative differences in potassium transport in proximal and distal segments of rat colon, unidirectional 22Na and 36Cl fluxes were performed under short-circuit conditions across isolated proximal colon of control and sodium-depleted rats with secondary hyperaldosteronism. In the control group, net sodium absorption (JNanet) (7.4 +/- 0.5 mu eq/h . cm2) was greater than Isc (1.4 +/- 0.1 mu eq/h . cm2), and JClnet was 0 in Ringer solution. Residual flux (JR) was -5.2 +/- 0.5 mu eq/h . cm2 consistent with hydrogen ion secretion suggesting that neutral sodium absorption may represent sodium-hydrogen exchange. 1 mM mucosal amiloride, which inhibits sodium-hydrogen exchange in other epithelia, produced comparable decreases in JNanet and JR (4.1 +/- 0.6 and 3.2 +/- 0.6 mu eq/h . cm2, respectively) without a parallel fall in Isc. Sodium depletion stimulated JNanet, JClnet, and Isc by 7.0 +/- 1.4, 6.3 +/- 1.9, and 0.8 +/- 0.2 mu eq/h . cm2, respectively, and 1 mM amiloride markedly inhibited JNanet and JClnet by 6.0 +/- 1.1 and 4.0 +/- 1.6 mu eq/h . cm2, respectively, with only a minimal reduction in Isc. Conclusions: the predominant neutral sodium-absorptive mechanism in proximal colon is sodium-hydrogen exchange. Sodium depletion stimulates electroneutral chloride-dependent sodium absorption (most likely as a result of increasing sodium-hydrogen and chloride-bicarbonate exchanges), not electrogenic chloride-independent sodium transport. The model of ion transport in the proximal colon is distinct from that of the distal colon.
机译:建议用于结肠的钠和氯的转运模型是基于在远端段进行的研究,并默认假定整个结肠的离子转运相似。在大鼠远端结肠中,中性氯化钠吸收占总钠吸收的主要部分,而醛固酮刺激电致阿米洛利敏感的钠离子吸收。由于我们已经证明了大鼠结肠近端和远端部分钾转运的质量差异,因此在短路条件下,对孤立的对照组和钠耗竭性继发性醛固酮过多症大鼠的近端结肠进行了短路条件下的单向22Na和36Cl通量处理。在对照组中,净钠吸收量(JNanet)(7.4 +/- 0.5μeq/ h。cm2)大于Isc(1.4 +/- 0.1μeq/ h。cm2),在林格溶液中,JClnet为0。残留通量(JR)为-5.2 +/- 0.5μeq / h。 cm2与氢离子分泌一致,表明中性钠吸收可能代表钠氢交换。 1 mM粘膜阿米洛利可抑制其他上皮细胞的钠氢交换,在JNanet和JR中可比的下降(分别为4.1 +/- 0.6和3.2 +/- 0.6μeq / h。cm2),而Isc却没有平行下降。钠消耗以7.0 +/- 1.4、6.3 +/- 1.9和0.8 +/- 0.2μeq / h刺激JNanet,JClnet和Isc。 cm2和1 mM阿米洛利分别抑制JNanet和JClnet 6.0 +/- 1.1和4.0 +/- 1.6μeq/ h。 cm2,而Isc的减小幅度很小。结论:近端结肠中主要的中性钠吸收机制是钠-氢交换。钠的消耗会刺激电子中性氯化物依赖性的钠吸收(最可能是由于钠-氢和氯离子-碳酸氢根交换增加的结果),而不是电离氯的钠离子转运。近端结肠中离子迁移的模型不同于远端结肠中的离子迁移的模型。

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