TRPA1 Channel Activation With Cinnamaldehyde Induces Cutaneous Vasodilation Through NOS, but Not COX and KCa Channel, Mechanisms in Humans.


Journal

Journal of cardiovascular pharmacology
ISSN: 1533-4023
Titre abrégé: J Cardiovasc Pharmacol
Pays: United States
ID NLM: 7902492

Informations de publication

Date de publication:
01 03 2022
Historique:
received: 22 07 2021
accepted: 06 11 2021
pubmed: 6 1 2022
medline: 30 4 2022
entrez: 5 1 2022
Statut: ppublish

Résumé

Transient receptor potential ankyrin 1 (TRPA1) channel activation induces cutaneous vasodilation in humans in vivo. However, the mechanisms underlying this response remains equivocal. We hypothesized that nitric oxide synthase (NOS) and Ca2+ activated K+ (KCa) channels contribute to the TRPA1 channel-induced cutaneous vasodilation with no involvement of cyclooxygenase (COX). Cutaneous vascular conductance (CVC) in 9 healthy young adults was assessed at 4 dorsal forearm skin sites treated by intradermal microdialysis with (1) 1.985% dimethyl sulfoxide + 0.015% lactated Ringer solution with propylene glycol (vehicle control), (2) 10 mM l-NAME, a nonselective NOS inhibitor, (3) 10 mM ketorolac, a nonselective COX inhibitor, or (4) 50 mM tetraethylammonium, a nonselective KCa channel blocker. Cinnamaldehyde, a TRPA1 channel activator, was administered to each skin site in a dose-dependent manner (2.9%, 8.8%, 26%, and 80%, each lasting ≥30 minutes). Administration of ≥8.8% cinnamaldehyde increased CVC from baseline at the vehicle control site by as much as 27.4% (95% confidence interval of 5.3; P < 0.001). NOS inhibitor attenuated the cinnamaldehyde-induced increases in CVC at the 8.8%, 26%, and 80% concentrations relative to the vehicle control site (all P ≤ 0.05). In contrast, both the COX inhibitor and KCa channel blockers did not attenuate the cinnamaldehyde induced-increases in CVC relative to the vehicle control site for all concentrations (all P ≥ 0.130). We conclude that in human skin in vivo, NOS plays a role in modulating the regulation of cutaneous vasodilation in response to TRPA1 channel activation with no detectable contributions of COX and KCa channels.

Identifiants

pubmed: 34983913
doi: 10.1097/FJC.0000000000001188
pii: 00005344-202203000-00016
doi:

Substances chimiques

Cyclooxygenase Inhibitors 0
TRPA1 Cation Channel 0
TRPA1 protein, human 0
Transient Receptor Potential Channels 0
Nitric Oxide 31C4KY9ESH
Acrolein 7864XYD3JJ
Nitric Oxide Synthase EC 1.14.13.39
Prostaglandin-Endoperoxide Synthases EC 1.14.99.1
cinnamaldehyde SR60A3XG0F

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

375-382

Informations de copyright

Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.

Déclaration de conflit d'intérêts

The authors report no conflicts of interest.

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Auteurs

Yufuko Kataoka (Y)

Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan.

Glen P Kenny (GP)

Human and Environmental Physiology Research Unit, University of Ottawa, Ottawa, Ontario, Canada.

Takeshi Nishiyasu (T)

Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan.

Tatsuro Amano (T)

Laboratory for Exercise and Environmental Physiology, Faculty of Education, Niigata University, Niigata, Japan.

Toby Mündel (T)

School of Sport Exercise and Nutrition, Massey University, Palmerston North, New Zealand; and.

Huixin Zheng (H)

School of Sport Exercise and Nutrition, Massey University, Palmerston North, New Zealand; and.

Tze-Huan Lei (TH)

College of Physical Education, Hubei Normal University, Huangshi, China.

Koichi Watanabe (K)

Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan.

Naoto Fujii (N)

Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan.

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