ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010
T-type Ca(2+) channel modulation by otilonium bromide.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Stalling the Enemy: Targeting Nsp13 for Next-Generation SARS-CoV-2 Antivirals.International journal of molecular sciences · 2026Article
- Otilonium bromide boosts antimicrobial activities of colistin against Gram-negative pathogens and their persisters.Communications biology · 2022Article
- Structure, gating, and pharmacology of human CaNature communications · 2022Article
- Effects of the Calcium Channel Blocker Otilonium Bromide on Seizure Activity in Rats With Pentylenetetrazole-Induced Convulsions.Neurochemical research · 2021Article
- Mechanotransduction in gastrointestinal smooth muscle cells: role of mechanosensitive ion channels.American journal of physiology. Gastrointestinal and liver physiology · 2021Review
- Experimental Models of Irritable Bowel Syndrome and the Role of the Enteric Neurotransmission.Journal of clinical medicine · 2018Review
- Modelling Human Colonic Smooth Muscle Cell Electrophysiology.Cellular and molecular bioengineering · 2017Article
- Changes in nitrergic and tachykininergic pathways in rat proximal colon in response to chronic treatment with otilonium bromide.Neurogastroenterology and motility · 2015Article
- Colonic smooth muscle cells and colonic motility patterns as a target for irritable bowel syndrome therapy: mechanisms of action of otilonium bromide.Therapeutic advances in gastroenterology · 2014Review
- Long-term efficacy and safety of otilonium bromide in the management of irritable bowel syndrome: a literature review.Clinical and experimental gastroenterology · 2014Review
- IBS and the role of otilonium bromide.International journal of colorectal disease · 2013Review
- Article
- Targeting ion channels for the treatment of gastrointestinal motility disorders.Therapeutic advances in gastroenterology · 2012Article
- The evaluation of otilonium bromide treatment in asian patients with irritable bowel syndrome.Journal of neurogastroenterology and motility · 2011Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Antispasmodics are used clinically to treat a variety of gastrointestinal disorders by inhibition of smooth muscle contraction. The main pathway for smooth muscle Ca(2+) entry is through L-type channels; however, there is increasing evidence that T-type Ca(2+) channels also play a role in regulating contractility. Otilonium bromide, an antispasmodic, has previously been shown to inhibit L-type Ca(2+) channels and colonic contractile activity. The objective of this study was to determine whether otilonium bromide also inhibits T-type Ca(2+) channels. Whole cell currents were recorded by patch-clamp technique from HEK293 cells transfected with cDNAs encoding the T-type Ca(2+) channels, Ca(V)3.1 (alpha1G), Ca(V)3.2 (alpha1H), or Ca(V)3.3 (alpha1I) alpha subunits. Extracellular solution was exchanged with otilonium bromide (10(-8) to 10(-5) M). Otilonium bromide reversibly blocked all T-type Ca(2+) channels with a significantly greater affinity for Ca(V)3.3 than Ca(V)3.1 or Ca(V)3.2. Additionally, the drug slowed inactivation in Ca(V)3.1 and Ca(V)3.3. Inhibition of T-type Ca(2+) channels may contribute to inhibition of contractility by otilonium bromide. This may represent a new mechanism of action for antispasmodics and may contribute to the observed increased clinical effectiveness of antispasmodics compared with selective L-type Ca(2+) channel blockers.
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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.