caa a22 4500 606235116 CHVBK 20210128101241.0 cr unu---uuuuu 210128e20150101xx s 000 0 eng 10.1007/s11010-014-2221-1 doi (NATIONALLICENCE)springer-10.1007/s11010-014-2221-1 The inhibitory effect of angiotensin II on BKCa channels in podocytes via oxidative stress [Elektronische Daten] [Na Gao, Hui Wang, Xiaochen Zhang, Zhuo Yang] Angiotensin II (Ang II) is an important active substance of the renin-angiotensin system (RAS). The present study has confirmed that abnormalities of Ang II may be related with cerebrovascular diseases, endocrine diseases, cardiovascular diseases, liver diseases, such as: cerebral hypoxia, diabetes, obesity, atrial fibrillation, and liver cirrhosis. However, understanding effects of Ang II on podocytes is not enough. This study was to investigate the effects of oxidative stress on the large conductance, Ca2+-activated K+ channels (BKCa). Results from the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay showed that Ang II induced podocyte death in a concentration-dependent manner. The measurement of superoxide dismutase (SOD) generation demonstrated that Ang II decreased the total SOD of cellular levels. Meaningfully, pretreatment of a type of ROS scavenger formulations named N-(mercaptopropionyl)-glycine (N-MPG) could inhibit podocyte apoptosis induced by Ang II. Meanwhile, patch-clamp technique was used in this study to detect the effects of Ang II on currents of BKCa channel in podocytes. The results indicated that Ang II inhibited the current amplitude of BKCa channel and decreased the slope of I-V curve. Ang II also made the activation curves of BKCa channel shift to the left. These results may provide a theoretical basis for potential treatment of chronic glomerular disease in the future. Springer Science+Business Media New York, 2014 Angiotensin II nationallicence Podocytes nationallicence BKCa channel nationallicence Patch-clamp technique nationallicence ROS nationallicence Gao Na School of Medicine, State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Tumor Microenvironment and Neurovascular Regulation, Nankai University, 300071, Tianjin, China aut Wang Hui Life Science Institute, Nankai University, 300071, Tianjin, China aut Zhang Xiaochen School of Medicine, State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Tumor Microenvironment and Neurovascular Regulation, Nankai University, 300071, Tianjin, China aut Yang Zhuo School of Medicine, State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Tumor Microenvironment and Neurovascular Regulation, Nankai University, 300071, Tianjin, China aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 398/1-2(2015-01-01), 217-222 0300-8177 398:1-2<217 2015 398 11010 https://doi.org/10.1007/s11010-014-2221-1 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-014-2221-1 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Gao Na School of Medicine, State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Tumor Microenvironment and Neurovascular Regulation, Nankai University, 300071, Tianjin, China aut NATIONALLICENCE 700 1- Wang Hui Life Science Institute, Nankai University, 300071, Tianjin, China aut NATIONALLICENCE 700 1- Zhang Xiaochen School of Medicine, State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Tumor Microenvironment and Neurovascular Regulation, Nankai University, 300071, Tianjin, China aut NATIONALLICENCE 700 1- Yang Zhuo School of Medicine, State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Tumor Microenvironment and Neurovascular Regulation, Nankai University, 300071, Tianjin, China aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 398/1-2(2015-01-01), 217-222 0300-8177 398:1-2<217 2015 398 11010