ArticleMolecular and cellular biochemistry2015
The inhibitory effect of angiotensin II on BKCa channels in podocytes via oxidative stress.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Mechanisms of angiotensin II to induce depression in diabetes.Diabetology international · 2025Review
- Role of angiotensin II in cellular entry and replication of dengue virus.Archives of virology · 2024Review
- Angiotensin II and post-streptococcal glomerulonephritis.Clinical and experimental nephrology · 2024Review
- Lipotoxicity-Related Hematological Disorders in Obesity.Advances in experimental medicine and biology · 2024Review
- Angiotensin II and dengue.Archives of virology · 2023Review
- Upregulation of NADH/NADPH oxidase 4 by angiotensin II induces podocyte apoptosis.Kidney research and clinical practice · 2023Article
- BKInternational journal of endocrinology · 2020Article
- Oxidative stress, autophagy and airway ion transport.American journal of physiology. Cell physiology · 2019Review
- Molecular Mechanisms Underlying Renin-Angiotensin-Aldosterone System Mediated Regulation of BK Channels.Frontiers in physiology · 2017Review
- Large-Conductance Calcium-Activated Potassium Channels in Glomerulus: From Cell Signal Integration to Disease.Frontiers in physiology · 2016Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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, Ca(2+)-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.
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