ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Caffeine relaxes smooth muscle through actin depolymerization.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 47 citations in OpenAlex.
- Bitter Taste Receptors 38 and 46 Regulate Intestinal Peristalsis.International journal of molecular sciences · 2025Article
- Contractile responses of engineered humanAPL bioengineering · 2024Article
- Ex Vivo Study of Colon Health, Contractility and Innervation in Male and Female Rats after Regular Exposure to Instant Cascara Beverage.Foods (Basel, Switzerland) · 2024Article
- Antispasmodic Activity of Light-Roasted Coffee Extract and Its Potential Use in Gastrointestinal Motility Disorders.Foods (Basel, Switzerland) · 2024Article
- Characterisation of Lipoma-Preferred Partner as a Novel Mechanotransducer in Vascular Smooth Muscle Cells.Cells · 2023Article
- Caffeine Induces G0/G1 Cell Cycle Arrest and Inhibits Migration through Integrin αv, β3, and FAK/Akt/c-Myc Signaling Pathway.Molecules (Basel, Switzerland) · 2021Article
- An update on extra-oral bitter taste receptors.Journal of translational medicine · 2021Review
- Review
- Elucidation of Cellular Mechanisms That Regulate the Sustained Contraction and Relaxation of the Mammalian Iris.Investigative ophthalmology & visual science · 2020Article
- Mast cells in asthma: Here I am, stuck in the middle with you.The European respiratory journal · 2020Article
- A new DNA marker CafLess-TCS1 for selection of caffeine-less tea plants.Breeding science · 2019Article
- Bitter Taste Receptors for Asthma Therapeutics.Frontiers in physiology · 2019Article
- Roles of airway smooth muscle dysfunction in chronic obstructive pulmonary disease.Journal of translational medicine · 2018Review
- Phenylephrine, a common cold remedy active ingredient, suppresses uterine contractions through cAMP signalling.Scientific reports · 2018Article
- Caffeine in Kidney Stone Disease: Risk or Benefit?Advances in nutrition (Bethesda, Md.) · 2018Review
- Extraoral bitter taste receptors in health and disease.The Journal of general physiology · 2017Review
- Marketed drugs used for the management of hypercholesterolemia as anticancer armament.OncoTargets and therapy · 2017Review
- Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Structure-Bioactivity Relationships of Methylxanthines: Trying to Make Sense of All the Promises and the Drawbacks.Molecules (Basel, Switzerland) · 2016Review
- Caffeine impairs gastrointestinal function in newborn rats.Pediatric research · 2015Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Caffeine is sometimes used in cell physiological studies to release internally stored Ca(2+). We obtained evidence that caffeine may also act through a different mechanism that has not been previously described and sought to examine this in greater detail. We ruled out a role for phosphodiesterase (PDE) inhibition, since the effect was 1) not reversed by inhibiting PKA or adenylate cyclase; 2) not exacerbated by inhibiting PDE4; and 3) not mimicked by submillimolar caffeine nor theophylline, both of which are sufficient to inhibit PDE. Although caffeine is an agonist of bitter taste receptors, which in turn mediate bronchodilation, its relaxant effect was not mimicked by quinine. After permeabilizing the membrane using β-escin and depleting the internal Ca(2+) store using A23187, we found that 10 mM caffeine reversed tone evoked by direct application of Ca(2+), suggesting it functionally antagonizes the contractile apparatus. Using a variety of molecular techniques, we found that caffeine did not affect phosphorylation of myosin light chain (MLC) by MLC kinase, actin-filament motility catalyzed by MLC kinase, phosphorylation of CPI-17 by either protein kinase C or RhoA kinase, nor the activity of MLC-phosphatase. However, we did obtain evidence that caffeine decreased actin filament binding to phosphorylated myosin heads and increased the ratio of globular to filamentous actin in precontracted tissues. We conclude that, in addition to its other non-RyR targets, caffeine also interferes with actin function (decreased binding by myosin, possibly with depolymerization), an effect that should be borne in mind in studies using caffeine to probe excitation-contraction coupling in smooth muscle.
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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.