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Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
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ATP-mediated release of arachidonic acid metabolites from venular endothelium causes arteriolar dilation

L W Hammer1, A L Ligon, R L Hester

  • 1Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505, USA. lhammer@physiology.umsmed.edu

American Journal of Physiology. Heart and Circulatory Physiology
|May 18, 2001
PubMed

Insights

Adenosine triphosphate (ATP) administered to venules causes adjacent arterioles to dilate. This vasodilation is endothelium-dependent and mediated by cyclooxygenase products, suggesting a role for ATP in regulating vascular tone.

Area of Science:

  • Physiology
  • Vascular Biology
  • Pharmacology

Background:

  • Endothelium-derived factors play a crucial role in regulating vascular tone.
  • Adenosine triphosphate (ATP) is recognized as a signaling molecule in the vasculature.
  • The precise mechanisms by which venular ATP influences arteriolar diameter are not fully elucidated.

Purpose of the Study:

  • To investigate if venular ATP administration induces endothelium-dependent dilation of adjacent arterioles.
  • To determine if cyclooxygenase (COX) products mediate the vasodilatory response to venular ATP.
  • To elucidate the role of the venular endothelium in ATP-induced vasodilation.

Main Methods:

  • In vivo microscopy was used to measure arteriolar diameter in anesthetized golden hamsters.
  • Adenosine triphosphate (ATP) was infused into venules, and subsequent arteriolar dilation was recorded.
  • The venular endothelium was disrupted using air bubbles, and the effect of ATP was re-evaluated.
  • Cyclooxygenase inhibition was achieved using indomethacin to assess its role in the response.

Main Results:

  • Venular ATP infusion caused significant dilation of adjacent arterioles (51 ± 4 to 76 ± 6 µm).
  • Disruption of the venular endothelium abolished the vasodilatory response to ATP.
  • Indomethacin significantly attenuated the arteriolar dilation induced by venular ATP.
  • Resting arteriolar diameter was not affected by endothelium disruption or indomethacin treatment.

Conclusions:

  • Venular administration of ATP stimulates the release of cyclooxygenase products.
  • These COX products, likely originating from the venular endothelium, mediate the dilation of adjacent arterioles.
  • ATP plays a role in regulating vascular tone through an endothelium-dependent, COX-mediated pathway.

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