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Extracellular calcium chelation and attenuation of calcium entry decrease in vivo cholinergic-induced eccrine

Kristen Metzler-Wilson1, Dawn L Sammons, Megan A Ossim

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This study shows that blocking calcium entry into sweat glands reduces their sensitivity to acetylcholine in human skin. This finding is important for understanding eccrine sweating mechanisms in vivo.

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Area of Science:

  • Physiology
  • Dermatology
  • Pharmacology

Background:

  • Calcium ions (Ca2+) are crucial second messengers in eccrine sweat gland function.
  • While internal and external calcium sources are known in vitro, their role in vivo in non-glabrous human skin remains unclear.
  • Understanding extracellular Ca2+ modulation is key to understanding sweat rate regulation.

Purpose of the Study:

  • To investigate if modulating extracellular Ca2+ levels affects sweat rate in non-glabrous human skin.
  • To determine if blocking Ca2+ influx through L-type channels impacts acetylcholine-induced sweating.
  • To translate findings from in vitro animal studies to in vivo human physiology.

Main Methods:

  • Acetylcholine (ACh) dose-response sweating was measured using capacitance hygrometry in healthy subjects.
  • Protocol 1 involved intradermal microdialysis of a Ca2+ chelator (EDTA) to lower interstitial Ca2+.
  • Protocol 2 used a Ca2+ channel blocker (verapamil) to inhibit L-type Ca2+ channels.

Main Results:

  • EDTA treatment significantly right-shifted the ACh dose-response curve, indicating reduced cholinergic sensitivity.
  • Verapamil also caused a significant right-shift in the ACh dose-response curve.
  • Neither EDTA nor verapamil altered the maximal sweat rate, suggesting a role in sensitivity rather than capacity.

Conclusions:

  • Local in vivo Ca2+ chelation and L-type Ca2+ channel blockade attenuate the cholinergic sensitivity of eccrine sweat glands.
  • Interstitial Ca2+ and its influx via Ca2+ channels play a functional role in eccrine sweating in intact non-glabrous human skin.
  • These findings provide in vivo evidence for calcium's role in regulating human sweat response.