ArticlePloS one2015
Propofol causes vasodilation in vivo via TRPA1 ion channels: role of nitric oxide and BKCa channels.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Sedation Strategy, Procedural Comfort, and Clinically Detected Radial Artery Spasm During Transradial Coronary Angiography: A Prospective Observational Study.Journal of clinical medicine · 2026Article
- The Influence of Anesthetics on the Functions of the Endothelium and Oxidative Stress: A Critical Review.Biomedicines · 2025Review
- TRPA1 Polymorphisms Modify the Hypotensive Responses to Propofol with No Change in Nitrite or Nitrate Levels.Current issues in molecular biology · 2022Article
- Arginase II polymorphisms modify the hypotensive responses to propofol by affecting nitric oxide bioavailability.European journal of clinical pharmacology · 2021Article
- Inhibition of Ligand-Gated TRPA1 by General Anesthetics.Molecular pharmacology · 2020Article
- Acute and chronic vascular effects of inhaled crotonaldehyde in mice: Role of TRPA1.Toxicology and applied pharmacology · 2020Article
- Novel Expression of GABAA Receptors on Resistance Arteries That Modulate Myogenic Tone.Journal of vascular research · 2020Article
- Transient Receptor Potential Ankyrin Type-1 Channels as a Potential Target for the Treatment of Cardiovascular Diseases.Frontiers in physiology · 2020Review
- TRPA1 channel contributes to myocardial ischemia-reperfusion injury.American journal of physiology. Heart and circulatory physiology · 2019Article
- Identification of molecular mechanism underlying therapeutic effect of tanshinone IIA in the treatment of hypoxic vestibular vertigo via the NO/cGMP/BKCa signaling pathway.American journal of translational research · 2019Article
- Formaldehyde Induces Mesenteric Artery Relaxation via a Sensitive Transient Receptor Potential Ankyrin-1 (TRPA1) and Endothelium-Dependent Mechanism: Potential Role in Postprandial Hyperemia.Frontiers in physiology · 2019Article
- Propofol-induced vasodilation of mesenteric arterioles via BKExperimental and therapeutic medicine · 2018Article
- c-Jun N-Terminal Kinases (JNKs) in Myocardial and Cerebral Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2018Review
- Sites Contributing to TRPA1 Activation by the Anesthetic Propofol Identified by Photoaffinity Labeling.Biophysical journal · 2017Article
- Identification of a putative binding site critical for general anesthetic activation of TRPA1.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- TRPA1 and TRPV1 contribute to propofol-mediated antagonism of U46619-induced constriction in murine coronary arteries.PloS one · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTransient receptor potential (TRP) ion channels of the A1 (TRPA1) and V1 (TRPV1) subtypes are key regulators of vasomotor tone. Propofol is an intravenous anesthetic known to cause vasorelaxation. Our objectives were to examine the extent to which TRPA1 and/or TRPV1 ion channels mediate propofol-induced depressor responses in vivo and to delineate the signaling pathway(s) involved.
methodsMice were subjected to surgery under 1.5-2.5% sevoflurane gas with supplemental oxygen. After a stable baseline in mean arterial pressure (MAP) was achieved propofol (2.5, 5.0, 10.0 mg/kg/min) was administered to assess the hemodynamic actions of the intravenous anesthetic. The effect of nitric oxide synthase (NOS) inhibition with L-NAME and/or calcium-gated K+ channel (BKCa) inhibition with Penetrim A (Pen A), alone and in combination, on propofol-induced decreases in mean arterial pressure were assessed in control C57Bl/6J, TRPA1-/-, TRPV1-/- and double-knockout mice (TRPAV-/-).
resultsPropofol decreased MAP in control mice and this effect was markedly attenuated in TRPA1-/- and TRPAV-/- mice but unaffected in TRPV1-/-mice. Moreover, pretreatment with L-NAME or Pen A attenuated the decrease in MAP in control and TRPV1-/- mice, and combined inhibition abolished the depressor response. In contrast, the markedly attenuated propofol-induced depressor response observed in TRPA1-/- and TRPAV-/- mice was unaffected by pre-treatment with Pen A or L-NAME when used either alone or in combination.
conclusionThese data demonstrate for the first time that propofol-induced depressor responses in vivo are predominantly mediated by TRPA1 ion channels with no involvement of TRPV1 ion channels and includes activation of both NOS and BKCa channels.
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