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首页> 外文期刊>Cellular Physiology and Biochemistry >Genistein potentiates the ANP effect on a K(+-)conductance in HEK-293 cells
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Genistein potentiates the ANP effect on a K(+-)conductance in HEK-293 cells

机译：金雀异黄素增强ANP对HEK-293细胞中K（+）电导的影响

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HEK-293 cells are known to reflect many features of the late distal tubule. Furthermore, they have the ability to release urodilatin, the structural analog to AN P. RTPCR was performed to test for the expression of natriuretic peptide receptors. While the mRNA for the human ANP receptor (NPR-A, GC-A) could be amplified, the CNP-specific receptor NPR-B (GC-B) and the receptor specific for guanylins, GC-C, could not be detected. In patch clamp experiments the effects of ANP (10 nM) on membrane voltage (V-m) were monitored and HEK-293 cells depolarized by 2.3 +/- 0.5 mV (n = 14). In the presence of the EGF receptor blocker genistein (10 muM) the effect of ANP was increased by 65% to 3.9 +/- 0.8 mV (n = 14). After removal of genistein the ANP-mediated depolarization further increased by 147% to 5.7 +/- 1.0 mV (n = 14). ANP given repetitively without genistein had no increasing depolarizing effect in HEK-293 cells with time. The ANP effect could be fully blocked by 1 muM Ba2+ and by 1 muM of the specific PKG inhibitor KT5823 indicating that ANP inhibits a K+-conductance via a cGMP-dependent protein kinase. Genistein itself hyperpolarized the membrane voltage of HEK-293 cells by -3.9 +/- 0.6 mV (n = 11) and this effect could also be fully blocked by Ba2+ (-0.3 +/- 0.1 mV, n = 5), indicating that genistein activates a K+-conductance which contributes significantly to the membrane potential of HEK-293 cells. Copyright (C) 2003 S. Karger AG, Basel. [References: 23]
机译：已知HEK-293细胞可反映晚期远端小管的许多特征。此外，它们具有释放尿苷素的能力，尿苷素是AN P的结构类似物。进行了RTPCR以测试利钠肽受体的表达。虽然可以扩增人ANP受体的mRNA（NPR-A，GC-A），但无法检测到CNP特异性受体NPR-B（GC-B）和鸟苷特异性受体GC-C。在膜片钳实验中，监测ANP（10 nM）对膜电压（V-m）的影响，并将HEK-293细胞去极化2.3 +/- 0.5 mV（n = 14）。在存在EGF受体阻断剂染料木黄酮（10μM）的情况下，ANP的作用提高了65％，达到3.9 +/- 0.8 mV（n = 14）。去除染料木黄酮后，ANP介导的去极化进一步增加了147％，达到5.7 +/- 1.0 mV（n = 14）。随时间推移，不加染料木黄酮重复给予的ANP在HEK-293细胞中没有增加的去极化作用。 1μMBa2 +和1μM特异性PKG抑制剂KT5823可以完全阻断ANP的作用，表明ANP通过cGMP依赖性蛋白激酶抑制K +传导。 Genistein本身使HEK-293细胞的膜电压超极化-3.9 +/- 0.6 mV（n = 11），Ba2 +（-0.3 +/- 0.1 mV，n = 5）也可以完全阻断这种作用，表明金雀异黄素激活K +电导，这极大地促进了HEK-293细胞的膜电位。版权所有（C）2003 S.Karger AG，巴塞尔。 [参考：23]

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