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Related Experiment Videos

Nucleoside-induced arteriolar constriction: a mast cell-dependent response

M P Doyle1, J Linden, B R Duling

  • 1Department of Molecular Physiology, University of Virginia Health Sciences Center, Charlottesville 22908.

The American Journal of Physiology
|May 1, 1994
PubMed
Summary
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Adenosine and inosine cause vasoconstriction in hamster cheek pouch arterioles, mediated by mast cell degranulation, not A1-receptor stimulation.

Area of Science:

  • Pharmacology
  • Physiology
  • Microcirculation

Background:

  • Adenosine (Ado) is known as a vasodilator, but can paradoxically cause vasoconstriction.
  • Constriction is often linked to A1-receptor stimulation or the renin-angiotensin system.

Purpose of the Study:

  • To investigate a novel vasoconstrictor action of adenosine and inosine in hamster cheek pouch arterioles.
  • To elucidate the underlying mechanism of nucleoside-induced vasoconstriction.

Main Methods:

  • Dissection and cannulation of hamster cheek pouch arterioles.
  • Measurement of luminal diameter changes in response to adenosine and inosine.
  • Pharmacological inhibition of adenosine receptors, uptake, deaminase, and mast cell degranulation.

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Main Results:

  • Adenosine induced a biphasic response: transient constriction at 10(-6) M, followed by dilation at higher concentrations.
  • A1-receptor antagonist did not affect constriction; inhibition of adenosine uptake abolished it.
  • Mast cell degranulation, evidenced by methylene blue staining, correlated with constriction.
  • Cromolyn blocked constriction, while compound 48/80 mimicked it.

Conclusions:

  • Adenosine and inosine induce vasoconstriction in arterioles via a mechanism independent of A1-receptors.
  • Mast cell degranulation plays a critical role in this nucleoside-induced vasoconstrictor response.
  • This study reveals a novel pathway for adenosine-mediated vasoconstriction involving mast cells.