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Related Experiment Videos

Decrease in vascular TxA2 receptors in a subgroup of rabbits unresponsive to a TxA2 mimetic

C J Buzzard1, S L Pfister, P V Halushka

  • 1Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas 75235.

The American Journal of Physiology
|June 1, 1994
PubMed
Summary

Some rabbits lack vascular responses to thromboxane A2 (TxA2) due to reduced TxA2 receptor density. This difference in TxA2 receptor expression may be regulated in vivo and offers a model for vascular disease research.

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Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Receptor Biology

Background:

  • Endothelium-dependent contractions in rabbit pulmonary arteries are mediated by thromboxane A2 (TxA2).
  • TxA2 mimetics, norepinephrine, and endothelin induce endothelium-independent contractions.
  • A subset of rabbits (25%) exhibit non-responsiveness to arachidonic acid, methacholine, and TxA2 mimetics.

Purpose of the Study:

  • To investigate the mechanism behind non-responsiveness to TxA2 in a subgroup of rabbits.
  • To characterize TxA2 receptor characteristics in responder versus non-responder rabbits.
  • To determine if the non-responsiveness is specific to the pulmonary artery.

Main Methods:

  • Vascular contraction studies using isolated rabbit pulmonary arteries and aortas.

Related Experiment Videos

  • Administration of arachidonic acid, methacholine, U-46619, norepinephrine, and endothelin.
  • Equilibrium binding studies using 125I-labeled I-BOP to assess TxA2 receptor affinity (Kd) and density (Bmax) in crude arterial membranes.
  • Platelet aggregation assays.

    • Main Results:

    • Non-responder arteries and aortas failed to contract in response to TxA2 agonists (arachidonic acid, methacholine, U-46619, I-BOP) but responded normally to norepinephrine and endothelin.
    • Binding studies revealed no significant difference in TxA2 receptor affinity (Kd) between responders and non-responders.
    • A significant decrease in TxA2 receptor density (Bmax) was observed in non-responder pulmonary arteries and aortas compared to responders (P < 0.01).
    • Non-responder platelets showed normal aggregation in response to U-46619, indicating preserved platelet TxA2 receptors.

    Conclusions:

    • The non-responsiveness to TxA2 in a subset of rabbits is associated with a reduced density of TxA2 receptors in vascular smooth muscle, not altered receptor affinity.
    • This phenomenon is not specific to the pulmonary artery, as demonstrated by similar findings in the aorta.
    • The findings suggest that TxA2 receptor expression may be regulated in vivo, and non-responder rabbits represent a valuable model for studying TxA2 receptor function in vascular disease.