Premium
The Effect of ET A and ET B Receptor Inhibition on Cutaneous Vasodilation and Sweating in Young Males During Rest and Exercise in the Heat
Author(s) -
Singh Maya,
Halili Lyra,
Fujii Naoto,
Kenny Glen P
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1290.17
Subject(s) - microdialysis , vasodilation , thermoregulation , chemistry , endothelin receptor , endothelin 1 , receptor , endocrinology , medicine , sweat , nitric oxide , sweat gland , central nervous system
During heat stress, increases in cutaneous blood flow and sweating are the main avenues by which a stable core body temperature can be maintained. However, the mechanisms underlying these responses remain elusive. Endothelin‐1 (ET‐1) is a powerful vasoconstrictor that can activate both endothelin A (ET A ) and endothelin B (ET B ) receptor subtypes, which contribute to the cutaneous vasodilation response induced by local skin heating. Additionally, both receptors are found on the human eccrine sweat glands. Given that ET A receptor activation can reduce nitric oxide (NO) bioavailability, which is known to augment both cutaneous vasodilation and sweating, we evaluated the hypothesis that the activation of ET A receptors may attenuate cutaneous vasodilation and sweating during heat stress. In this study, eight males (25 ± 4 years) performed an intermittent cycling protocol on a semi‐recumbent bicycle consisting of two 30 min bouts of moderate (40% VO 2 max) and high (75% VO 2 max) intensity exercise in the heat (35°C); separated by a 20‐ and 40‐ min recovery period respectively. Cutaneous vascular conductance (CVC, laser‐Doppler perfusion units/mean arterial pressure), normalized to maximal CVC, and sweat rate (ventilated capsule) were evaluated at four intradermal microdialysis forearm skin sites. Each site was perfused with either 1) lactated Ringer (Control), 2) 500 n M BQ‐123 (a selective ET A receptor blocker), 3) 300 n M BQ‐788 (a selective ET B receptor blocker), or 4) a combination of BQ‐123 and BQ‐788. During both exercise bouts, relative to Control (Exercise 1: 47 ± 8% max ; Exercise 2: 62 ± 1% max ), there were no between‐site differences in CVC (all P > 0.05). However, at the end of each recovery period, the blockade of ET A receptors (Recovery 1: 49 ± 4% max ; Recovery 2: 49 ± 3% max ) and the dual blockade of ET A and ET B receptors (Recovery 1: 49 ± 7% max ; Recovery 2: 57 ± 8% max ) augmented CVC in comparison to Control (Recovery 1: 33 ± 6% max ; Recovery 2: 39 ± 5% max ; P < 0.05). We observed no between‐site differences in sweat rate throughout the protocol from baseline rest to the end of the second recovery (all P > 0.05). We show that neither ET A nor ET B receptors modulate cutaneous perfusion and sweating during exercise in the heat. Furthermore, we demonstrate that activation of ET A receptors reduces cutaneous perfusion during passive heat stress after exercise in the heat. Support or Funding Information This study was supported by grants from the Natural Sciences and Engineering Research Council of Canada (Discover grant, RGPIN‐06313‐2014; Discovery Grants Program ‐ Accelerator Supplement, RGPAS‐462252‐2014; funds held by Dr. Glen P. Kenny).