ArticleScientific reports2016
Hydrophobic bile acids relax rat detrusor contraction via inhibiting the opening of the Na⁺/Ca²⁺ exchanger.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- The Cardiomyocyte in Cirrhosis: Pathogenic Mechanisms Underlying Cirrhotic Cardiomyopathy.Reviews in cardiovascular medicine · 2024Review
- Bile Acids as Inducers of Protonophore and Ionophore Permeability of Biological and Artificial Membranes.Membranes · 2023Review
- TGR5 agonists induce peripheral and central hypersensitivity to bladder distension.Scientific reports · 2022Article
- Increased transient receptor potential canonical 3 activity is involved in the pathogenesis of detrusor overactivity by dynamic interaction with NaLaboratory investigation; a journal of technical methods and pathology · 2022Article
- Involvement of oxidative species in cyclosporine-mediated cholestasis.Frontiers in pharmacology · 2022Review
- TGR5 Expression Is Associated with Changes in the Heart and Urinary Bladder of Rats with Metabolic Syndrome.Life (Basel, Switzerland) · 2021Article
- Gene Expressions Underlying Mishandled Calcium Clearance and Elevated Generation of Reactive Oxygen Species in the Coronary Artery Smooth Muscle Cells of Chronic Heart Failure Rats.Chinese medical journal · 2017Article
- Investigation of triamterene as an inhibitor of the TGR5 receptor: identification in cells and animals.Drug design, development and therapy · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hydrophobic bile acids (BAs) are thought to inhibit smooth muscle contractility in several organs. The present study was undertaken to investigate the effects of hydrophobic BAs on the detrusor contractility of rat bladder and to explore the possible mechanism. Lithocholic acid (LCA) treatment increased the micturition interval and induced a concentration-dependent relaxation of bladder detrusor strips. In addition, LCA reduced the concentration of intracellular free Ca(2+)([Ca(2+)]i) and inhibited both the outward and inward Na(+)/Ca(2+) exchanger (NCX) current (INCX) in primary isolated smooth muscle cells (SMCs). To further investigate the mechanism of action of LCA, several pharmacologic agents were used. We found that the NCX inhibitor 3',4'-Dichlorobenzamil (DCB) can significantly inhibit the relaxation of detrusor strips and a reduction of the [Ca(2+)]i induced by LCA, while the antagonist of muscarinic receptor and the agonist of the G protein-coupled bile acid receptor (TGR5) and the farnesoid X receptor (FXR) had no effect. In conclusion, these data suggest that the relaxation of rat detrusor induced by hydrophobic BAs is mediated by NCX. Further research is needed to carry out to demonstrate the possible pathway and provide a potential new strategy to investigation for the treatment of the low urinary tract syndromes.
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