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不依赖血管加压素的肾脏尿液浓缩:rBSC1增加及逆流倍增增强。

Vasopressin-independent renal urinary concentration: increased rBSC1 and enhanced countercurrent multiplication.

作者信息

Michimata Mari, Mizukami Kazuhiko, Suzuki Michiko, Kazama Itsuro, Nakamura Yohsuke, Suzuki Katsuya, Yanagisawa Teruyuki, Imai Yutaka, Sasaki Sei, Matsubara Mitsunobu

机构信息

Department of Molecular Medicine and Gene Transfer Research, Tohoku University School of Medicine, Sendai, Japan.

出版信息

Kidney Int. 2003 Sep;64(3):933-8. doi: 10.1046/j.1523-1755.2003.00182.x.

DOI:10.1046/j.1523-1755.2003.00182.x
PMID:12911543
Abstract

BACKGROUND

A close association between the expression of the sodium transporter, rat bumetanide sensitive cotransporter (rBSC), in thick ascending limb of Henle and urinary concentration has been reported. However, direct evidence for this association and the mechanism of rBSC1 expression are still to be elucidated.

METHODS

Brattleboro (BB) rats weighing approximately 200 g were dehydrated by water restriction for 4 hours, which induced around a 5% body weight reduction. Although plasma arginine vasopressin (AVP) was undetectable even after the water restriction, BB rats concentrated urine from 182 +/- 23 (mean +/- SD) at baseline to 404 +/- 65 mOsm/kg. H2O.

RESULTS

Urinary volume was reduced from 5.8 +/- 1.8 to 1.4 +/- 0.6 mL/h. This treatment significantly increased sodium and urea accumulation in the renal medulla and reduced urinary sodium excretion. rBSC1 signals for both mRNA and protein were increased in dehydrated rats, although aquaporin type 2 (AQP2) expression was not enhanced in dehydrated BB rats. Subcutaneous infusion of desmopressin acetate (DDAVP) intensified rBSC1 signals of BB rats more than those in dehydrated condition.

CONCLUSION

Dehydration increased rBSC1 expression and enhanced countercurrent multiplication even in AVP deficiency. These results supply strong evidence for the association between rBSC1 expression and urinary concentration, and indicate the presence of an AVP-independent mechanism for urine concentration.

摘要

背景

已有报道称,亨利氏袢升支粗段中钠转运体——大鼠布美他尼敏感共转运体(rBSC)的表达与尿液浓缩之间存在密切关联。然而,这种关联的直接证据以及rBSC1表达的机制仍有待阐明。

方法

对体重约200克的布拉特洛维(BB)大鼠进行限水脱水4小时,导致体重减轻约5%。尽管限水后血浆精氨酸加压素(AVP)无法检测到,但BB大鼠的尿液浓缩能力从基线时的182±23(平均值±标准差)毫渗量/千克·H₂O提高到了404±65毫渗量/千克·H₂O。

结果

尿量从5.8±1.8毫升/小时降至1.4±0.6毫升/小时。该处理显著增加了肾髓质中钠和尿素的蓄积,并减少了尿钠排泄。脱水大鼠中rBSC1的mRNA和蛋白质信号均增加,尽管脱水的BB大鼠中2型水通道蛋白(AQP2)的表达未增强。皮下注射醋酸去氨加压素(DDAVP)比脱水状态下更增强了BB大鼠的rBSC1信号。

结论

即使在AVP缺乏的情况下,脱水也会增加rBSC1的表达并增强逆流倍增。这些结果为rBSC1表达与尿液浓缩之间的关联提供了有力证据,并表明存在一种不依赖AVP的尿液浓缩机制。

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