ArticleBritish journal of pharmacology2000
Bile acids increase intracellular Ca(2+) concentration and nitric oxide production in vascular endothelial cells.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 62 citations in OpenAlex.
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- "Gut Microbiota as a Therapeutic Target for Hypertension: Challenges and Insights for Future Clinical Applications" "Gut Microbiota and Hypertension Therapy".Current hypertension reports · 2025Review
- Bile Acid Application in Cell-Targeting for Molecular Receptors in Relation to Hearing: A Comprehensive Review.Current drug targets · 2024Review
- Deoxycholic Acid, a Secondary Bile Acid, Increases Cardiac Output and Blood Pressure in Rats.Nutrients · 2023Article
- The Dynamic Role of Endoplasmic Reticulum Stress in Chronic Liver Disease.The American journal of pathology · 2023Review
- Article
- The Role of Bile Acids in the Human Body and in the Development of Diseases.Molecules (Basel, Switzerland) · 2022Review
- Bile acids and salt-sensitive hypertension: a role of the gut-liver axis.American journal of physiology. Heart and circulatory physiology · 2022Review
- [Review of Research Progress in Biliary Substitutes].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021Review
- Diphlorethohydroxycarmalol Isolated fromInternational journal of molecular sciences · 2021Article
- Overview of bile acid signaling in the cardiovascular system.World journal of clinical cases · 2021Review
- Bile Acids, Liver Cirrhosis, and Extrahepatic Vascular Dysfunction.Frontiers in physiology · 2021Review
- Acute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data.PloS one · 2021Article
- Article
- Serum Metabonomics Analysis of Liver Failure Treated by Nonbioartificial Liver Support Systems.Canadian journal of gastroenterology & hepatology · 2018Article
- The involvement of endoplasmic reticulum stress in bile acid-induced hepatocellular injury.Journal of clinical biochemistry and nutrition · 2014Article
- Article
- Bile acids regulate cardiovascular function.Clinical and translational science · 2011Review
- Embryonic stem cell-derived cardiomyocytes as a model to study fetal arrhythmia related to maternal disease.Journal of cellular and molecular medicine · 2009Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of bile acids on intracellular Ca(2+) concentration [Ca(2+)](i) and nitric oxide production were investigated in vascular endothelial cells. Whole-cell patch clamp techniques and fluorescence measurements of [Ca(2+)](i) were applied in vascular endothelial cells obtained from human umbilical and calf aortic endothelial cells. Nitric oxide released was determined by measuring the concentration of NO(2)(-). Deoxycholic acid, chenodeoxycholic acid and the taurine conjugates increased [Ca(2+)](i) concentration-dependently, while cholic acid showed no significant effect. These effects resulted from the first mobilization of Ca(2+) from an inositol 1,4,5-triphosphate (IP(3))-sensitive store, which was released by ATP, then followed by Ca(2+) influx. Both bile acids and ATP induced the activation of Ca(2+)-dependent K(+) current. Oscillations of [Ca(2+)](i) were occasionally monitored with the Ca(2+)-dependent K(+) current in voltage-clamped cells and Ca(2+) measurements of single cells. The intracellular perfusion of heparin completely abolished the ATP effect, but failed to inhibit the bile acid effect. Deoxycholic acid and chenodeoxycholic acid enhanced NO(2)(-) production concentration-dependently, while cholic acid did not enhance it. The bile acids-induced nitric oxide production was suppressed by N(G)-nitro-L-arginine methyl ester, exclusion of extracellular Ca(2+) or N-(6-aminohexyl)-5-chloro-l-naphthalenesulphonamide hydrochloride (W-7) and calmidazolium, calmodulin inhibitors. These results provide novel evidence showing that bile acids increase [Ca(2+)](i) and subsequently nitric oxide production in vascular endothelial cells. The nitric oxide production induced by bile acids may be involved in the pathogenesis of circulatory abnormalities in liver diseases including cirrhosis.
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Registered trials
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