Exogenous Activation of Protease-Activated Receptor 2 Attenuates Cutaneous Vasodilatation and Sweating in Older Men Exercising in the Heat.


Journal

Skin pharmacology and physiology
ISSN: 1660-5535
Titre abrégé: Skin Pharmacol Physiol
Pays: Switzerland
ID NLM: 101188418

Informations de publication

Date de publication:
2019
Historique:
received: 03 03 2019
accepted: 26 04 2019
pubmed: 21 6 2019
medline: 29 1 2020
entrez: 21 6 2019
Statut: ppublish

Résumé

Protease-activated receptor 2 (PAR2) exists in the cutaneous vasculature and eccrine sweat glands. We previously showed that in young habitually active men, exogenous PAR2 activation via the agonist SLIGKV-NH2 had no effect on heat loss responses of cutaneous vasodilatation and sweating during rest or exercise in the heat. However, ageing is associated with altered mechanisms governing these responses. Thus, the effect of exogenous PAR2 activation on cutaneous vasodilatation and sweating in older individuals may differ from that in young adults. Local cutaneous vascular conductance (CVC) and sweat rate were measured in 9 older males (62 ± 4 years) at four forearm skin sites treated with the following: (1) lactated Ringer solution (control), (2) 0.05 mM, (3) 0.5 mM, or (4) 5 mM SLIGKV-NH2. Measurements were performed while participants rested in a non-heat-stress environment (25°C) for ∼60 min and an additional 50 min thereafter in the heat (40°C). Participants then performed 50 min of cycling at a fixed metabolic heat load of 200 W/m2 (to maintain the same thermal drive for heat loss between participants) followed by a 30-min recovery. CVC during non-heat-stress resting was elevated from the control site with 5 mM SLIGKV-NH2 (p ≤ 0.05), but this response was not observed during ambient heat exposure. By contrast, 5 mM SLIGKV-NH2 lowered CVC during the early stage (10 and 20 min) of exercise compared to the control site (all p ≤ 0.05). Although sweating during non-heat-stressed and heat-stressed resting was not affected by any dose of SLIGKV-NH2, it was reduced with all SLIGKV-NH2 doses relative to the control site during and following exercise (all p ≤ 0.05). We show that while exogenous PAR2 activation induces cutaneous vasodilatation at rest under non-heat-stressed conditions, it attenuates cutaneous vasodilatation and sweating during and following an exercise-induced heat stress in older men.

Sections du résumé

BACKGROUND BACKGROUND
Protease-activated receptor 2 (PAR2) exists in the cutaneous vasculature and eccrine sweat glands. We previously showed that in young habitually active men, exogenous PAR2 activation via the agonist SLIGKV-NH2 had no effect on heat loss responses of cutaneous vasodilatation and sweating during rest or exercise in the heat. However, ageing is associated with altered mechanisms governing these responses. Thus, the effect of exogenous PAR2 activation on cutaneous vasodilatation and sweating in older individuals may differ from that in young adults.
METHODS METHODS
Local cutaneous vascular conductance (CVC) and sweat rate were measured in 9 older males (62 ± 4 years) at four forearm skin sites treated with the following: (1) lactated Ringer solution (control), (2) 0.05 mM, (3) 0.5 mM, or (4) 5 mM SLIGKV-NH2. Measurements were performed while participants rested in a non-heat-stress environment (25°C) for ∼60 min and an additional 50 min thereafter in the heat (40°C). Participants then performed 50 min of cycling at a fixed metabolic heat load of 200 W/m2 (to maintain the same thermal drive for heat loss between participants) followed by a 30-min recovery.
RESULTS RESULTS
CVC during non-heat-stress resting was elevated from the control site with 5 mM SLIGKV-NH2 (p ≤ 0.05), but this response was not observed during ambient heat exposure. By contrast, 5 mM SLIGKV-NH2 lowered CVC during the early stage (10 and 20 min) of exercise compared to the control site (all p ≤ 0.05). Although sweating during non-heat-stressed and heat-stressed resting was not affected by any dose of SLIGKV-NH2, it was reduced with all SLIGKV-NH2 doses relative to the control site during and following exercise (all p ≤ 0.05).
CONCLUSION CONCLUSIONS
We show that while exogenous PAR2 activation induces cutaneous vasodilatation at rest under non-heat-stressed conditions, it attenuates cutaneous vasodilatation and sweating during and following an exercise-induced heat stress in older men.

Identifiants

pubmed: 31220834
pii: 000500643
doi: 10.1159/000500643
doi:

Substances chimiques

F2RL1 protein, human 0
Oligopeptides 0
Receptor, PAR-2 0
seryl-leucyl-isoleucyl-glycyl-lysyl-valinamide 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

235-243

Informations de copyright

© 2019 S. Karger AG, Basel.

Auteurs

Naoto Fujii (N)

Human and Environmental Physiology Research Unit, University of Ottawa, Ottawa, Ontario, Canada, fujii.naoto.gb@u.tsukuba.ac.jp.
Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan, fujii.naoto.gb@u.tsukuba.ac.jp.

Kion Hatam (K)

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

Gregory W McGarr (GW)

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

Robert D Meade (RD)

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

Pierre Boulay (P)

Faculty of Physical Activity Sciences, University of Sherbrooke, Sherbrooke, Québec, Canada.

Takeshi Nishiyasu (T)

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.

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Classifications MeSH