Decreased renal perfusion rapidly increases plasma membrane Na-K-ATPase in rat cortex by an angiotensin II-dependent mechanism.
Decreased renal perfusion rapidly increases plasma membrane Na-K-ATPase in rat cortex by an angiotensin II-dependent mechanism.
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肾灌注减少通过血管紧张素 II 依赖性机制迅速增加大鼠皮质中的质膜 Na-K-ATP 酶。
DOI：
10.1152/ajprenal.90363.2008
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Beierwaltes,WilliamH
中科院分区：
文献类型：
--
作者：
Yingst,DouglasR;Araghi,Ali;Doci,TabithaM;Mattingly,Raymond;Beierwaltes,WilliamH
为了了解血压的快速变化如何调节肾皮质中的Na-K-ATPase，我们检验了一种假说，即短期(5分钟)肾灌流压降低会通过血管紧张素II依赖的机制增加质膜上的Na-K-ATPase的数量。麻醉SD大鼠采用肾动脉间结扎法缩窄腹主动脉，在急性缩窄时监测两侧压力。左肾灌注压降至70±1 mm Hg(n=6)，右肾灌注压为112±4 mm Hg(n=6)。对照组(非狭窄)大鼠(n=5)双侧肾脏压力相似，为119±6 mm Hg。减少灌注量5min后，取股静脉血测血浆肾素活性(PRA)，切取肾脏。大脑皮层被解剖、切碎、筛分和生物素标记。低灌注量左肾较右肾质膜Na-K-ATPase增加41%(P<；0.003)。对照组左右肾细胞表面Na-K-ATPase差异无统计学意义(P=0.47)。与对照组相比，实验动物的PRA升高了57%。为了验证血管紧张素II在调节Na-K-ATPase升高中的作用，我们在雷米普利拉治疗的大鼠上重复了实验(n=6)。当血管紧张素转换酶被抑制时，两肾细胞表面Na-K-ATPase相等(P=0.46)。这一结果证实了我们的假设：血压的快速变化调节了Na-K-ATPase在肾皮质的转运。
To understand how rapid changes in blood pressure can regulate Na-K-ATPase in the kidney cortex, we tested the hypothesis that a short-term (5 min) decrease in renal perfusion pressure will increase the amount of Na-K-ATPase in the plasma membranes by an angiotensin II-dependent mechanism. The abdominal aorta of anesthetized Sprague-Dawley rats was constricted with a ligature between the renal arteries, and pressure was monitored on either side during acute constriction. Left renal perfusion pressure was reduced to 70 ± 1 mmHg (n= 6), whereas right renal perfusion pressure was 112 ± 4 mmHg. In control (nonconstricted) rats (n= 5), pressure to both kidneys was similar at 119 ± 6 mmHg. After 5 min of reduced perfusion, femoral venous samples were taken for plasma renin activity (PRA) and the kidneys excised. The cortex was dissected, minced, sieved, and biotinylated. Lower perfusion left kidneys showed a 41% increase (P< 0.003) in the amount of Na-K-ATPase in the plasma membrane compared with right kidneys. In controls, there was no difference in cell surface Na-K-ATPase between left and right kidneys (P= 0.47). PRA was 57% higher in experimental animals compared with controls. To test the role of angiotensin II in mediating the increase in Na-K-ATPase, we repeated the experiments (n= 6) in rats treated with ramiprilat. When angiotensin-converting enzyme was inhibited, the cell surface Na-K-ATPase of the two kidneys was equal (P=0.46).These results confirm our hypothesis: rapid changes in blood pressure regulate trafficking of Na-K-ATPase in the kidney cortex.
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DOI：
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