Inhibitory effect of ETB receptor on Na(+)-K(+) ATPase activity by extracellular Ca(2+) entry and Ca(2+) release from the endoplasmic reticulum in renal proximal tubule cells.
Inhibitory effect of ETB receptor on Na(+)-K(+) ATPase activity by extracellular Ca(2+) entry and Ca(2+) release from the endoplasmic reticulum in renal proximal tubule cells.
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DOI：
10.1038/hr.2009.112
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发表时间：
2009-10
影响因子：
5.4
通讯作者：
Zeng, Chunyu
中科院分区：
文献类型：
--
作者：
Liu, Yan;Yang, Jian;Ren, Hongmei;He, Duofen;Pascua, Annabelle;Armando, M. Ines;Yang, Chengming;Zhou, Lin;Felder, Robin A.;Jose, Pedro A.;Zeng, Chunyu
肾脏在血压和钠稳态的长期调节中很重要。肾脏中ETB受体的刺激增加钠排泄，部分是通过减少Henle氏延髓粗升支和集合管中的钠转运。然而，ETB受体对肾近曲小管（RPT）细胞Na+-K+ ATP酶活性的作用尚不清楚。本研究旨在验证ETB受体抑制大鼠RPT细胞Na ~+-K ~+ ATP酶活性的假说，并探讨其作用机制。在Wistar-Kyoto大鼠RPT细胞中，ETB受体激动剂BQ 3020刺激ETB受体，通过ATP水解测定Na+-K+ ATP酶活性降低（对照=0.38±0.02，BQ 3020 =0.26±0.03，BQ 788 =0.40±0.06，BQ 3020 + BQ 788 =0.37±0.04，n=5，P<0.01）。ETB受体介导的Na+-K+ ATP酶活性抑制依赖于细胞内钙的增加，因为这种作用被细胞内游离钙螯合剂（BAPTA-AM; 5×10−3 m 15 min−1）、钙通道阻滞剂（10−6 m 15 min−1尼卡地平）和PI 3激酶抑制剂（10−7 m/渥曼青霉素）消除。肌醇1，4，5-三磷酸（IP 3）受体阻断剂（2-氨基乙基二苯基硼酸酯; 10−4 m 15 min−1）也阻断了ETB受体对Na+-K+ ATP酶活性的抑制作用（对照组=0.39±0.06，BQ 3020 =0.25±0.01，2-APB=0.35±0.05，BQ 3020 + 2-APB = 0.35±0.06，n=4，P<0.01）。钙通道激动剂（BAY-K8644; 10−6 m 15 min−1）抑制Na+-K+ ATP酶活性，这种作用可被磷脂酰肌醇-3激酶抑制剂（10−7 m 15 min−1渥曼青霉素）阻断。在大鼠RPT细胞中，ETB受体的激活通过促进细胞外Ca 2+进入和Ca 2+从内质网释放来抑制Na+-K+ ATP酶活性。
The kidney is important in the long-term regulation of blood pressure and sodium homeostasis. Stimulation of ETB receptors in the kidney increases sodium excretion, in part, by decreasing sodium transport in the medullary thick ascending limb of Henle and in collecting duct. However, the role of ETB receptor on Na+–K+ ATPase activity in renal proximal tubule (RPT) cells is not well defined. The purpose of this study is to test the hypothesis that ETB receptor inhibits Na+–K+ ATPase activity in rat RPT cells, and investigate the mechanism(s) by which such an action is produced. In RPT cells from Wistar–Kyoto rats, stimulation of ETB receptors by the ETB receptor agonist, BQ3020, decreased Na+–K+ ATPase activity, determined by ATP hydrolysis (control=0.38±0.02, BQ3020=0.26±0.03, BQ788=0.40±0.06, BQ3020+BQ788=0.37±0.04, n=5, P<0.01). The ETB receptor-mediated inhibition of Na+–K+ ATPase activity was dependent on an increase in intracellular calcium, because this effect was abrogated by a chelator of intracellular-free calcium (BAPTA-AM; 5×10−3 m 15 min−1), Ca2+ channel blocker (10−6 m 15 min−1 nicardipine) and PI3 kinase inhibitor (10−7 m per wortmannin). An inositol 1,4,5-trisphosphate (IP3) receptor blocker (2-aminoethyl diphenyl borate; 10−4 m 15 min−1) also blocked the inhibitory effect of the ETB receptor on Na+–K+ ATPase activity (control=0.39±0.06, BQ3020=0.25±0.01, 2-APB=0.35±0.05, BQ3020+ 2-APB=0.35±0.06, n=4, P<0.01). The calcium channel agonist (BAY-K8644; 10−6 m 15 min−1) inhibited Na+–K+ ATPase activity, an effect that was blocked by a phosphatidylinositol-3 kinase inhibitor (10−7 m 15 min−1 wortmannin). In rat RPT cells, activation of the ETB receptor inhibits Na+–K+ ATPase activity by facilitating extracellular Ca2+ entry and Ca2+ release from endoplasmic reticulum.
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DOI：
10.1152/ajpheart.2001.281.5.h2218
发表时间：
2001-11-01
影响因子：
4.8
作者：
Ballew, JR;Fink, GD
通讯作者：
Fink, GD
影响因子：
8.3
作者：
Li, XX;Bek, M;Jose, PA
通讯作者：
Jose, PA
影响因子：
4.5
作者：
Bouallegue, Ali;Daou, Grace Bou;Srivastava, Ashok K.
通讯作者：
Srivastava, Ashok K.
DOI：
10.1006/bbrc.2000.2724
发表时间：
2000-05-19
影响因子：
3.1
作者：
Chu, TS;Wu, KD;Hsieh, BS
通讯作者：
Hsieh, BS
影响因子：
3.4
作者：
Gutierrez-Martin, Y;Martin-Romero, FJ;Henao, F
通讯作者：
Henao, F