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The Mouse Cremaster Muscle Preparation for Intravital Imaging of the Microcirculation
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The Mouse Cremaster Muscle Preparation for Intravital Imaging of the Microcirculation

Published on: June 10, 2011

Multiple dilator pathways in skeletal muscle contraction-induced arteriolar dilations

Coral L Murrant1, Ingrid H Sarelius

  • 1Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|March 15, 2002
PubMed

Insights

Muscle contraction triggers arteriolar dilation through nitric oxide (NO), adenosine (Ado) receptors, and ATP-sensitive potassium (K(ATP)) channels locally. Upstream dilation involves K(ATP) channels and Ado receptors, but not NO.

Area of Science:

  • Physiology
  • Vascular Biology
  • Exercise Physiology

Background:

  • Muscle contraction is known to induce local and conducted arteriolar dilations.
  • The precise signaling pathways mediating these dilations, particularly the roles of nitric oxide (NO), adenosine (Ado) receptors, and ATP-sensitive potassium (K(ATP)) channels, remain incompletely understood.

Purpose of the Study:

  • To investigate the involvement of NO, Ado receptors, and K(ATP) channels in arteriolar dilations during muscle contraction.
  • To differentiate the roles of these mediators in local versus conducted (upstream) vasodilation.

Main Methods:

  • Utilized an in vivo cremaster muscle preparation in anesthetized hamsters.
  • Stimulated muscle fibers to induce contraction and measured arteriolar diameter changes at local and upstream sites.
  • Administered specific inhibitors: N(omega)-nitro-L-arginine (NO synthase inhibitor), xanthine amine congener (XAC; Ado receptor antagonist), and glibenclamide (Glib; K(ATP) channel inhibitor).

Main Results:

  • Muscle contraction induced significant local and upstream arteriolar dilations.
  • Local dilation was attenuated by NO synthase inhibition, Ado receptor antagonism, and K(ATP) channel blockade.
  • Upstream dilation was significantly attenuated by Ado receptor antagonism and K(ATP) channel blockade, but not by NO synthase inhibition.
  • Direct application of glibenclamide to the upstream site attenuated upstream dilation, suggesting a local role of K(ATP) channels at that site.

Conclusions:

  • Nitric oxide, adenosine receptors, and K(ATP) channels contribute to local arteriolar dilation initiated by muscle contraction.
  • K(ATP) channels and adenosine receptors, but not NO, are crucial for the upstream propagation of this dilation.

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