ArticlePflugers Archiv : European journal of physiology2014
Cinnamaldehyde inhibits L-type calcium channels in mouse ventricular cardiomyocytes and vascular smooth muscle cells.
Article in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed.
- Proof of Pharmacology, Safety, and Pharmacokinetics of the Novel TRPA1 Antagonist BI 1839100: A Randomized, Placebo-Controlled, Parallel Group, First-In-Human Study in Healthy Male Participants.Clinical and translational science · 2025Trial
- Effects of TRP channel agonist ingestion on metabolism and autonomic nervous system in a randomized clinical trial of healthy subjects.Scientific reports · 2016Trial
- Monoterpenes in Vascular Function: A Review of Bioactivity and Mechanisms of Action.International journal of molecular sciences · 2025Review
- The Impact of Maternal/In Utero Exposure of Novel Tobacco Products on the Offspring Cardiovascular Health.Cardiovascular toxicology · 2025Review
- Qualitative chemical analysis of cinnamon flavored e-cigarette vapor to identify compounds of interest that may affect cardiovascular function.microPublication biology · 2025Article
- Natural L-type calcium channels antagonists from Chinese medicine.Chinese medicine · 2024Article
- Functional Analysis of TRPA1, TRPM3, and TRPV1 Channels in Human Dermal Arteries and Their Role in Vascular Modulation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Cinnamon: a nutraceutical supplement for the cardiovascular system.Archives of medical sciences. Atherosclerotic diseases · 2024Article
- Unveiling the role of TRPA1 in cardiovascular health and disease: a mini review.Frontiers in cardiovascular medicine · 2024Review
- Trans-cinnamaldehyde protects against phenylephrine-induced cardiomyocyte hypertrophy through the CaMKII/ERK pathway.BMC complementary medicine and therapies · 2022Article
- Experimental Study on the Mechanism of Cinnamaldehyde Ameliorate Proteinuria Induced by Adriamycin.BioMed research international · 2022Article
- The Therapeutic Roles of Cinnamaldehyde against Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2022Review
- The Role of Essential Oils and Their Main Compounds in the Management of Cardiovascular Disease Risk Factors.Molecules (Basel, Switzerland) · 2021Review
- Review
- Review of Natural Resources With Vasodilation: Traditional Medicinal Plants, Natural Products, and Their Mechanism and Clinical Efficacy.Frontiers in pharmacology · 2021Review
- Comparative effects of parent and heated cinnamaldehyde on the function of human iPSC-derived cardiac myocytes.Toxicology in vitro : an international journal published in association with BIBRA · 2019Article
- The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits.Metabolic brain disease · 2019Article
- Cardiovascular Activity of the Chemical Constituents of Essential Oils.Molecules (Basel, Switzerland) · 2017Review
- Cinnamon effects on metabolic syndrome: a review based on its mechanisms.Iranian journal of basic medical sciences · 2016Review
- Cinnamon: Mystic powers of a minute ingredient.Pharmacognosy research · 2015Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cinnamaldehyde (CA), a major component of cinnamon, is known to have important actions in the cardiovascular system, including vasorelaxation and decrease in blood pressure. Although CA-induced activation of the chemosensory cation channel TRPA1 seems to be involved in these phenomena, it has been shown that genetic ablation of Trpa1 is insufficient to abolish CA effects. Here, we confirm that CA relaxes rat aortic rings and report that it has negative inotropic and chronotropic effects on isolated mouse hearts. Considering the major role of L-type Ca(2+) channels in the control of the vascular tone and cardiac contraction, we used whole-cell patch-clamp to test whether CA affects L-type Ca(2+) currents in mouse ventricular cardiomyocytes (VCM, with Ca(2+) as charge carrier) and in mesenteric artery smooth muscle cells (VSMC, with Ba(2+) as charge carrier). We found that CA inhibited L-type currents in both cell types in a concentration-dependent manner, with little voltage-dependent effects. However, CA was more potent in VCM than in VSMC and caused opposite effects on the rate of inactivation. We found these divergences to be at least in part due to the use of different charge carriers. We conclude that CA inhibits L-type Ca(2+) channels and that this effect may contribute to its vasorelaxing action. Importantly, our results demonstrate that TRPA1 is not a specific target of CA and indicate that the inhibition of voltage-gated Ca(2+) channels should be taken into account when using CA to probe the pathophysiological roles of TRPA1.
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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.