Acetylcholine released from cholinergic nerves contributes to cutaneous vasodilation during heat stress

Manabu Shibasaki, Thad E. Wilson, Jian Cui, Craig G. Crandall

Research output: Contribution to journalArticle

61 Citations (Scopus)

Abstract

Nitric oxide (NO) contributes to active cutaneous vasodilation during a heat stress in humans. Given that acetylcholine is released from cholinergic nerves during whole body heating, coupled with evidence that acetylcholine causes vasodilation via NO mechanisms, it is possible that release of acetylcholine in the dermal space contributes to cutaneous vasodilation during a heat stress. To test this hypothesis, in seven subjects skin blood flow (SkBF) and sweat rate were simultaneously monitored over three microdialysis membranes placed in the dermal space of dorsal forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine (10 μM), the second membrane was perfused with the NO synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME; 10 mM) dissolved in the aforementioned neostigmine solution (L-NAME Neo ), and the third membrane was perfused with Ringer solution as a control site. Each subject was exposed to ∼20 min of whole body heating via a water-perfused suit, which increased mean body temperature from 36.4 ± 0.1 to 37.5 = 0.1°C (P < 0.05). After the heat stress, SkBF at each site was normalized to its maximum value, identified by administration of 28 mM sodium nitroprusside. Mean body temperature threshold for cutaneous vasodilation was significantly lower at the neostigmine-treated site relative to the other sites (neostigmine: 36.6 ± 0.1°C, L-NAME Neo : 37.1 ± 0.1°C, control: 36.9 ± 0.1°C), whereas no significant threshold difference was observed between the L-NAME Neo -treated and control sites. At the end of the heat stress, SkBF was not different between the neostigmine-treated and control sites, whereas SkBF at the L-NAME Neo -treated site was significantly lower than the other sites. These results suggest that acetylcholine released from cholinergic nerves is capable of modulating cutaneous vasodilation via NO synthase mechanisms early in the heat stress but not after substantial cutaneous vasodilation.

Original languageEnglish (US)
Pages (from-to)1947-1951
Number of pages5
JournalJournal of Applied Physiology
Volume93
Issue number6
DOIs
StatePublished - Jan 1 2002

Fingerprint

Vasodilation
Cholinergic Agents
Acetylcholine
Neostigmine
Hot Temperature
Skin
NG-Nitroarginine Methyl Ester
Membranes
Body Temperature
Nitric Oxide Synthase
Heating
Nitric Oxide
Sweat
Cholinesterase Inhibitors
Microdialysis
Nitroprusside
Forearm

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Shibasaki, Manabu ; Wilson, Thad E. ; Cui, Jian ; Crandall, Craig G. / Acetylcholine released from cholinergic nerves contributes to cutaneous vasodilation during heat stress. In: Journal of Applied Physiology. 2002 ; Vol. 93, No. 6. pp. 1947-1951.
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abstract = "Nitric oxide (NO) contributes to active cutaneous vasodilation during a heat stress in humans. Given that acetylcholine is released from cholinergic nerves during whole body heating, coupled with evidence that acetylcholine causes vasodilation via NO mechanisms, it is possible that release of acetylcholine in the dermal space contributes to cutaneous vasodilation during a heat stress. To test this hypothesis, in seven subjects skin blood flow (SkBF) and sweat rate were simultaneously monitored over three microdialysis membranes placed in the dermal space of dorsal forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine (10 μM), the second membrane was perfused with the NO synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME; 10 mM) dissolved in the aforementioned neostigmine solution (L-NAME Neo ), and the third membrane was perfused with Ringer solution as a control site. Each subject was exposed to ∼20 min of whole body heating via a water-perfused suit, which increased mean body temperature from 36.4 ± 0.1 to 37.5 = 0.1°C (P < 0.05). After the heat stress, SkBF at each site was normalized to its maximum value, identified by administration of 28 mM sodium nitroprusside. Mean body temperature threshold for cutaneous vasodilation was significantly lower at the neostigmine-treated site relative to the other sites (neostigmine: 36.6 ± 0.1°C, L-NAME Neo : 37.1 ± 0.1°C, control: 36.9 ± 0.1°C), whereas no significant threshold difference was observed between the L-NAME Neo -treated and control sites. At the end of the heat stress, SkBF was not different between the neostigmine-treated and control sites, whereas SkBF at the L-NAME Neo -treated site was significantly lower than the other sites. These results suggest that acetylcholine released from cholinergic nerves is capable of modulating cutaneous vasodilation via NO synthase mechanisms early in the heat stress but not after substantial cutaneous vasodilation.",
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Acetylcholine released from cholinergic nerves contributes to cutaneous vasodilation during heat stress. / Shibasaki, Manabu; Wilson, Thad E.; Cui, Jian; Crandall, Craig G.

In: Journal of Applied Physiology, Vol. 93, No. 6, 01.01.2002, p. 1947-1951.

Research output: Contribution to journalArticle

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N2 - Nitric oxide (NO) contributes to active cutaneous vasodilation during a heat stress in humans. Given that acetylcholine is released from cholinergic nerves during whole body heating, coupled with evidence that acetylcholine causes vasodilation via NO mechanisms, it is possible that release of acetylcholine in the dermal space contributes to cutaneous vasodilation during a heat stress. To test this hypothesis, in seven subjects skin blood flow (SkBF) and sweat rate were simultaneously monitored over three microdialysis membranes placed in the dermal space of dorsal forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine (10 μM), the second membrane was perfused with the NO synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME; 10 mM) dissolved in the aforementioned neostigmine solution (L-NAME Neo ), and the third membrane was perfused with Ringer solution as a control site. Each subject was exposed to ∼20 min of whole body heating via a water-perfused suit, which increased mean body temperature from 36.4 ± 0.1 to 37.5 = 0.1°C (P < 0.05). After the heat stress, SkBF at each site was normalized to its maximum value, identified by administration of 28 mM sodium nitroprusside. Mean body temperature threshold for cutaneous vasodilation was significantly lower at the neostigmine-treated site relative to the other sites (neostigmine: 36.6 ± 0.1°C, L-NAME Neo : 37.1 ± 0.1°C, control: 36.9 ± 0.1°C), whereas no significant threshold difference was observed between the L-NAME Neo -treated and control sites. At the end of the heat stress, SkBF was not different between the neostigmine-treated and control sites, whereas SkBF at the L-NAME Neo -treated site was significantly lower than the other sites. These results suggest that acetylcholine released from cholinergic nerves is capable of modulating cutaneous vasodilation via NO synthase mechanisms early in the heat stress but not after substantial cutaneous vasodilation.

AB - Nitric oxide (NO) contributes to active cutaneous vasodilation during a heat stress in humans. Given that acetylcholine is released from cholinergic nerves during whole body heating, coupled with evidence that acetylcholine causes vasodilation via NO mechanisms, it is possible that release of acetylcholine in the dermal space contributes to cutaneous vasodilation during a heat stress. To test this hypothesis, in seven subjects skin blood flow (SkBF) and sweat rate were simultaneously monitored over three microdialysis membranes placed in the dermal space of dorsal forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine (10 μM), the second membrane was perfused with the NO synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME; 10 mM) dissolved in the aforementioned neostigmine solution (L-NAME Neo ), and the third membrane was perfused with Ringer solution as a control site. Each subject was exposed to ∼20 min of whole body heating via a water-perfused suit, which increased mean body temperature from 36.4 ± 0.1 to 37.5 = 0.1°C (P < 0.05). After the heat stress, SkBF at each site was normalized to its maximum value, identified by administration of 28 mM sodium nitroprusside. Mean body temperature threshold for cutaneous vasodilation was significantly lower at the neostigmine-treated site relative to the other sites (neostigmine: 36.6 ± 0.1°C, L-NAME Neo : 37.1 ± 0.1°C, control: 36.9 ± 0.1°C), whereas no significant threshold difference was observed between the L-NAME Neo -treated and control sites. At the end of the heat stress, SkBF was not different between the neostigmine-treated and control sites, whereas SkBF at the L-NAME Neo -treated site was significantly lower than the other sites. These results suggest that acetylcholine released from cholinergic nerves is capable of modulating cutaneous vasodilation via NO synthase mechanisms early in the heat stress but not after substantial cutaneous vasodilation.

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