ArticleBritish journal of pharmacology2005
Glibenclamide depletes ATP in renal proximal tubular cells by interfering with mitochondrial metabolism.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Intracellular Calcium Changes Correlate with Mitochondrial Dynamics After Differential Modulation of KATP Channels in a Cellular Model of Parkinson's Disease.Neurochemical research · 2025Article
- Glibenclamide Serves as a Potent Vasopressor to Treat Vasoplegia After Cardiopulmonary Bypass and Reperfusion in a Porcine Model.International journal of molecular sciences · 2025Article
- The impact of ATP-sensitive potassium channel modulation on mitochondria in a Parkinson's disease model using SH-SY5Y cells depends on their differentiation state.Journal of bioenergetics and biomembranes · 2024Article
- Validation of Freshly Isolated Rat Renal Cells as a Tool for Preclinical Assessment of Radiolabeled Receptor-Specific Peptide Uptake in the Kidney.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Impact of Membrane Voltage on Formation and Stability of Human Renal Proximal TubulesACS biomaterials science & engineering · 2022Article
- Article
- Comparison of two sulfonylureas with high and low myocardial K(ATP) channel affinity on myocardial infarct size and metabolism in a rat model of type 2 diabetes.Diabetologia · 2011Article
- Oxygen sensing and conducted vasomotor responses in mouse cremaster arterioles in situ.Pflugers Archiv : European journal of physiology · 2010Article
- Opening of the mitoKATP channel and decoupling of mitochondrial complex II and III contribute to the suppression of myocardial reperfusion hyperoxygenation.Molecular and cellular biochemistry · 2010Article
- Insulin-induced electrophysiology changes in human pleura are mediated via its receptor.Experimental diabetes research · 2010Article
- Sulfonylurea receptor-dependent and -independent pathways mediate vasodilation induced by ATP-sensitive K+ channel openers.Molecular pharmacology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sulfonylurea drugs, like glibenclamide, stimulate insulin secretion by blocking ATP-sensitive potassium channels on pancreatic beta cells. Renal tubular epithelial cells possess a different class of K(ATP) channels with much lower affinities for sulfonylurea drugs, necessitating the use of micromolar glibenclamide concentrations to study these channels. Here, we describe the toxic effects of these concentrations on mitochondrial energy metabolism in freshly isolated renal proximal tubular cells. Glibenclamide, at concentrations of 50 and 100 microM, reduced intracellular ATP levels by 28+/-4 and 53+/-5%, respectively (P<0.01). This decline in ATP could be attributed to a dose-dependent inhibition of mitochondrial respiration. Glibenclamide (10-500 microM) inhibited ADP-stimulated mitochondrial oxygen consumption. In addition to this toxic effect, specific association of radiolabeled and fluorescent glibenclamide to renal mitochondria was found. Association of [(3)H]glibenclamide with renal mitochondria revealed a low-affinity site with a K(D) of 16+/-6 microM and a B(max) of 167+/-29 pmol mg(-1). We conclude that micromolar concentrations of glibenclamide interfere with mitochondrial bioenergetics and, therefore, should be used with care for inhibition of epithelial K(ATP) channels.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.