ArticleThe Journal of clinical investigation1997
Angiotensin II depolarizes podocytes in the intact glomerulus of the Rat.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 91 citations in OpenAlex.
- Association of triglyceride glucose index with the risk of acute kidney injury in patients with coronary revascularization: a cohort study.Diabetology & metabolic syndrome · 2024Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Upregulated LRRC55 promotes BK channel activation and aggravates cell injury in podocytes.The Journal of experimental medicine · 2021Article
- Injured Podocytes Are Sensitized to Angiotensin II-Induced Calcium Signaling.Journal of the American Society of Nephrology : JASN · 2020Article
- Inhibition of Endocytosis of Clathrin-Mediated Angiotensin II Receptor Type 1 in Podocytes Augments Glomerular Injury.Journal of the American Society of Nephrology : JASN · 2019Article
- Molecular Mechanisms of Kidney Injury and Repair in Arterial Hypertension.International journal of molecular sciences · 2019Review
- Regulation and Function of TMEM16F in Renal Podocytes.International journal of molecular sciences · 2018Article
- Actin dynamics at focal adhesions: a common endpoint and putative therapeutic target for proteinuric kidney diseases.Kidney international · 2018Review
- Podocyte directed therapy of nephrotic syndrome-can we bring the inside out?Pediatric nephrology (Berlin, Germany) · 2016Review
- Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli.Journal of visualized experiments : JoVE · 2015Article
- Article
- The inhibitory effect of angiotensin II on BKCa channels in podocytes via oxidative stress.Molecular and cellular biochemistry · 2015Article
- The Hippo pathway is controlled by Angiotensin II signaling and its reactivation induces apoptosis in podocytes.Cell death & disease · 2014Article
- Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli.Kidney international · 2014Article
- Resistance to insulin and kidney disease in the cardiorenal metabolic syndrome; role for angiotensin II.Molecular and cellular endocrinology · 2013Review
- Single-channel analysis of TRPC channels in the podocytes of freshly isolated Glomeruli.Methods in molecular biology (Clifton, N.J.) · 2013Article
- ARB protects podocytes from HIV-1 nephropathy independently of podocyte AT1.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2012Article
- Calcium regulates podocyte actin dynamics.Seminars in nephrology · 2012Review
- Cell biology and pathology of podocytes.Annual review of physiology · 2012Review
- Obesity-related glomerulopathy and podocyte injury: a mini review.Frontiers in bioscience (Elite edition) · 2012Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to examine the effects of angiotensin II (Ang II) on cellular functions of rat podocytes (pod) in the intact freshly isolated glomerulus and in culture. Membrane voltage (Vm) and ion currents of pod were examined with the patch clamp technique in fast whole cell and whole cell nystatin configuration. Vm of pod was -38+/-1 mV (n = 86). Ang II led to a concentration-dependent depolarization of pod with an ED50 of 10(-8) mol/liter. In the presence of Ang II (10(-7) mol/liter, n = 20), pod depolarized by 7+/-1 mV. In an extracellular solution with a reduced Cl- concentration of 32 mmol/liter, the effect of Ang II on Vm was significantly increased to 14+/-4 mV (n = 8). The depolarization induced by Ang II was neither inhibited in an extracellular Na+-free solution nor in a solution with a reduced extracellular Ca2+ (down to 1 micromol/liter). Like Ang II, the calcium ionophore A23187 (10(-5) mol/liter, n = 9) depolarized pod by 10+/-2 mV, whereas forskolin (10(-5) mol/liter), 8-(4-chlorophenylthio)-cAMP and N2,2'-o-dibutyryl-cGMP (both 5 x 10(-4) mol/liter) did not alter Vm of pod. The angiotensin 1 receptor antagonist losartan (10(-7) mol/liter) completely inhibited the Ang II-induced (10(-7) mol/liter) depolarization (n = 5). Like pod in the glomerulus, pod in short term culture depolarized in response to Ang II (10(-8) mol/liter, n = 5). Our results suggest that Ang II depolarizes podocytes directly by opening a Cl- conductance. The activation of this ion conductance is mediated by an AT1 receptor and may be regulated by the intracellular Ca2+ activity.
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