Effect of vanadate on renal tubular function in rats.
Effect of vanadate on renal tubular function in rats.
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钒酸盐对大鼠肾小管功能的影响。
DOI：
10.1152/ajprenal.1981.240.6.f522
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Garcia,ME
中科院分区：
文献类型：
--
作者：
Westenfelder,C;Hamburger,RK;Garcia,ME
正钒酸盐（VO4）已被证明能引起大鼠明显的尿钠。这归因于其对肾脏na - k - atp酶活性的抑制作用。因为几乎所有的肾元段都具有na - k - atp酶活性，所以给药VO4会改变整个肾元的肾小管运输。为了检验这种可能性，成年大鼠被麻醉并注入VO4 （10 μ mol）。Kg体wt-1 - h-1静脉注射)。该剂量对肾小球滤过率、有效肾血浆流量和血压没有影响，而尿流量、钠和水排泄明显增加。钾排泄保持不变。VO4仅抑制最大的碳酸氢盐和葡萄糖的重吸收，而不会导致正常血糖或碳酸氢盐水平下的葡萄糖或碳酸氢盐“泄漏”。在急性甲状腺甲状旁腺切除的大鼠中，VO4产生了显著的磷尿，而不伴有肾源性cAMP排泄的增加。VO4显著抑制了Brattleboro大鼠的游离水清除率和正常大鼠的游离水重吸收。这些数据表明，VO4抑制近端和远端肾元段的肾小管重吸收。我们认为，VO4通过抑制na - k - atp酶活性来影响肾小管功能。
Orthovanadate (VO4) has been shown to cause a marked natriuresis in rats. This has been ascribed to its inhibitory action on renal Na-K-ATPase activity. Because virtually all nephron segments possess Na-K-ATPase activity the administration of VO4 should alter renal tubular transport along the entire nephron. To examine this possibility, adult rats were anesthetized and infused with VO4 (10 mumol.kg body wt-1.h-1 i.v.). This dose had no effect on glomerular filtration rate, effective renal plasma flow, and blood pressure, whereas urine flow and sodium and water excretion rose markedly. Potassium excretion remained unaltered. VO4 depressed only maximal bicarbonate and glucose reabsorption without causing a glucose or bicarbonate "leak" at normal levels of blood glucose or bicarbonate. In acutely thyroparathyroidectomized rats VO4 produced a striking phosphaturia, not accompanied by an increase in nephrogenous cAMP excretion. Both free water clearance in Brattleboro rats and free water reabsorption in normal rats was significantly depressed by VO4. These data demonstrate that VO4 depresses tubular reabsorption in proximal and distal nephron segments. We conclude that VO4 exerts its effect on tubular function by inhibition of Na-K-ATPase activity.