Cutaneous active vasodilation in humans is mediated by cholinergic nerve cotransmission

D. L. Kellogg, P. E. Pergola, K. L. Piest, W. A. Kosiba, C. G. Crandall, M. Grossmann, J. M. Johnson

Research output: Contribution to journalArticle

254 Citations (Scopus)

Abstract

During heat stress, increases in blood flow in nonglabrous skin in humans are mediated through active vasodilation by an unknown neurotransmitter mechanism. To investigate this mechanism, a three part study was performed to determine the following: (1) is muscarinic receptor activation necessary for active cutaneous vasodilation? We iontophoretically applied atropine to a small area of forearm skin. At that site and an untreated control site, we measured the vasomotor (laser-Doppler blood flow [LDF]) and sudomotor (relative humidity) responses to whole-body heat stress. Blood pressure was monitored. Cutaneous vascular conductance (CVC) was calculated (LDF-mean arterial pressure). Sweating was blocked at treated sites only. CVC rose at both sites (P<.05 at each site); thus, cutaneous active vasodilation is not effected through muscarinic receptors. (2) Are nonmuscarinic cholinergic receptors present on cutaneous arterioles? Acetylcholine (ACh was iontophoretically applied to forearm skin at sites pretreated by atropine iontophoresis and at untreated sites. ACh increased CVC at untreated sites (P<.05) but not at atropinized sites. Thus, the only functional cholinergic receptors on cutaneous vessels are muscarinic. (3) Does cutaneous active vasodilation involve cholinergic nerve cotransmission? Botulinum toxin was injected intradermally in the forearm to block release of ACh and any coreleased neurotransmitters. Heat stress was performed as in part I of the study. At treated sites, CVC and relative humidity remained at baseline levels during heat stress (P>.05). Active vasodilator and sudomotor responses to heat stress were abolished by botulinum toxin. We conclude that cholinergic nerve activation mediates cutaneous active vasodilation through release of an unknown cotransmitter, not through.

Original languageEnglish (US)
Pages (from-to)1222-1228
Number of pages7
JournalCirculation Research
Volume77
Issue number6
StatePublished - 1995

Fingerprint

Vasodilation
Cholinergic Agents
Skin
Blood Vessels
Lasers
Hot Temperature
Heat-Shock Response
Sweating
Botulinum Toxins
Muscarinic Receptors
Humidity
Vasodilator Agents
Atropine
Forearm
Neurotransmitter Agents
Arterial Pressure
Blood Pressure

Keywords

  • active vasodilation
  • cotransmitters
  • laser-Doppler flowmetry
  • muscarinic receptors
  • skin blood flow

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Kellogg, D. L., Pergola, P. E., Piest, K. L., Kosiba, W. A., Crandall, C. G., Grossmann, M., & Johnson, J. M. (1995). Cutaneous active vasodilation in humans is mediated by cholinergic nerve cotransmission. Circulation Research, 77(6), 1222-1228.

Cutaneous active vasodilation in humans is mediated by cholinergic nerve cotransmission. / Kellogg, D. L.; Pergola, P. E.; Piest, K. L.; Kosiba, W. A.; Crandall, C. G.; Grossmann, M.; Johnson, J. M.

In: Circulation Research, Vol. 77, No. 6, 1995, p. 1222-1228.

Research output: Contribution to journalArticle

Kellogg, DL, Pergola, PE, Piest, KL, Kosiba, WA, Crandall, CG, Grossmann, M & Johnson, JM 1995, 'Cutaneous active vasodilation in humans is mediated by cholinergic nerve cotransmission', Circulation Research, vol. 77, no. 6, pp. 1222-1228.
Kellogg DL, Pergola PE, Piest KL, Kosiba WA, Crandall CG, Grossmann M et al. Cutaneous active vasodilation in humans is mediated by cholinergic nerve cotransmission. Circulation Research. 1995;77(6):1222-1228.
Kellogg, D. L. ; Pergola, P. E. ; Piest, K. L. ; Kosiba, W. A. ; Crandall, C. G. ; Grossmann, M. ; Johnson, J. M. / Cutaneous active vasodilation in humans is mediated by cholinergic nerve cotransmission. In: Circulation Research. 1995 ; Vol. 77, No. 6. pp. 1222-1228.
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N2 - During heat stress, increases in blood flow in nonglabrous skin in humans are mediated through active vasodilation by an unknown neurotransmitter mechanism. To investigate this mechanism, a three part study was performed to determine the following: (1) is muscarinic receptor activation necessary for active cutaneous vasodilation? We iontophoretically applied atropine to a small area of forearm skin. At that site and an untreated control site, we measured the vasomotor (laser-Doppler blood flow [LDF]) and sudomotor (relative humidity) responses to whole-body heat stress. Blood pressure was monitored. Cutaneous vascular conductance (CVC) was calculated (LDF-mean arterial pressure). Sweating was blocked at treated sites only. CVC rose at both sites (P<.05 at each site); thus, cutaneous active vasodilation is not effected through muscarinic receptors. (2) Are nonmuscarinic cholinergic receptors present on cutaneous arterioles? Acetylcholine (ACh was iontophoretically applied to forearm skin at sites pretreated by atropine iontophoresis and at untreated sites. ACh increased CVC at untreated sites (P<.05) but not at atropinized sites. Thus, the only functional cholinergic receptors on cutaneous vessels are muscarinic. (3) Does cutaneous active vasodilation involve cholinergic nerve cotransmission? Botulinum toxin was injected intradermally in the forearm to block release of ACh and any coreleased neurotransmitters. Heat stress was performed as in part I of the study. At treated sites, CVC and relative humidity remained at baseline levels during heat stress (P>.05). Active vasodilator and sudomotor responses to heat stress were abolished by botulinum toxin. We conclude that cholinergic nerve activation mediates cutaneous active vasodilation through release of an unknown cotransmitter, not through.

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