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首页> 外文期刊>American Journal of Physiology >Decreased vasopressin-mediated renal water reabsorption in rats with compensated liver cirrhosis.
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Decreased vasopressin-mediated renal water reabsorption in rats with compensated liver cirrhosis.

机译：代偿性肝硬化大鼠中加压素介导的肾水重吸收减少。

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Experiments were performed to investigate vasopressin type 2 receptor (V2)-mediated renal water reabsorption and the renal expression of the vasopressin-regulated water channel aquaporin-2 (AQP-2) in cirrhotic rats with sodium retention but without ascites. In addition, the expression of the furosemide-sensitive type 1 Na-K-2Cl cotransporter (BSC-1) and the natriuretic response to an intravenous test dose furosemide (7.5 mg/kg) during acute V2-receptor blockade was measured. Acute V2-receptor blockade with the selective nonpeptide antagonist OPC-31260 (800 microg . kg-1 . h-1) was performed during conditions in which volume depletion was prevented by computer-driven, servo-controlled intravenous volume replacement with 150 mM glucose. OPC-31260 produced a significantly smaller increase in urine flow rate (-26%) and free water clearance (-18%) in cirrhotic rats than in control rats. The natriuretic response to an intravenous test dose furosemide (7.5 mg/kg) was significantly increased in cirrhotic rats (+52%), but pretreatment with OPC-31260 did not affect the natriuretic response to furosemide in neither cirrhotic nor in control rats. Semiquantitative immunoblotting showed a significant downregulation of AQP-2 in the renal cortex (-72%) and in the outer medulla (-44%). The relative expression of BSC-1 in the outer medulla was unchanged in cirrhotic rats. The corticopapillary gradient of Na was significantly increased in cirrhotic rats. Since daily urine flow rate was similar in cirrhotic and sham-operated rats, we suggest that non-vasopressin-mediated water reabsorption is increased in cirrhotic rats probably as a result of an increased corticomedullary gradient due to exaggerated NaCl reabsorption in the thick ascending limb of Henle's loop.
机译：进行实验以研究2型加压素（V2）介导的肾水重吸收以及肝硬化大鼠中有钠retention留但无腹水的加压素调节水通道Aquaporin-2（AQP-2）在肾脏中的表达。此外，在急性V2受体阻滞过程中，测量了速尿敏感性1型Na-K-2Cl共转运蛋白（BSC-1）的表达和对静脉注射速尿（7.5 mg / kg）的利钠尿反应。在通过计算机控制的伺服控制的静脉内体积置换术以150 mM葡萄糖预防体积减少的情况下，使用选择性非肽拮抗剂OPC-31260（800微克。kg-1。h-1）进行急性V2受体阻滞。与对照组大鼠相比，OPC-31260在肝硬化大鼠中产生的尿流率（-26％）和游离水清除率（-18％）显着减小。肝硬化大鼠对静脉注射剂量速尿（7.5 mg / kg）的利尿钠反应显着增加（+ 52％），但是用OPC-31260进行预处理既不会影响肝硬化大鼠，也不会影响对照大鼠对速尿的利尿钠反应。半定量免疫印迹显示肾皮质（-72％）和髓质外（-44％）的AQP-2明显下调。在肝硬化大鼠中，髓外层中BSC-1的相对表达没有变化。肝硬化大鼠的皮质乳头钠含量显着增加。由于肝硬化和假手术大鼠的每日尿流率相似，我们建议肝硬化大鼠中非血管加压素介导的水重吸收增加，可能是由于皮质的髓质梯度增加所致，这是由于在粗大上升肢中NaCl重吸收过大所致。亨利的循环。

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