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Daltroban blocks thromboxane responses in the pulmonary vascular bed of the cat

J S Hood1, B D Nossaman, I N Ibrahim

  • 1Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana 70112.

Insights

Daltroban selectively blocks thromboxane (Tx) A2 receptors in cat pulmonary vasculature. This agent reversibly inhibits TxA2 mimic responses without affecting other vasoactive substances, supporting distinct TxA2 receptors.

Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Pulmonary Circulation

Background:

  • Thromboxane (Tx) A2 is a potent vasoconstrictor.
  • The role of TxA2 receptors in pulmonary vascular responses requires further elucidation.
  • Daltroban is a selective TxA2 receptor antagonist.

Purpose of the Study:

  • To investigate the effects of daltroban on pulmonary vascular responses in cats.
  • To determine the selectivity of daltroban against TxA2 receptor-mediated vasoconstriction.
  • To explore the presence of distinct TxA2 receptors in the feline pulmonary vasculature.

Main Methods:

  • Intact-chest cat model with constant-flow pulmonary circulation.
  • Administration of daltroban (5 mg/kg iv).
  • Assessment of vascular pressure responses to TxA2 mimics (U-46619, U-44069), prostaglandins (PGF2α, PGD2, 9α,11β-PGF2), arachidonic acid, norepinephrine, serotonin, angiotensin II, BAY K 8644, endothelin peptides, and platelet-activating factor.

Main Results:

  • Daltroban significantly decreased responses to U-46619 and U-44069 without affecting responses to PGF2α, PGD2, or 9α,11β-PGF2.
  • Dose-response curves for TxA2 mimics were shifted rightward in a parallel manner.
  • Daltroban did not alter responses to norepinephrine, serotonin, angiotensin II, BAY K 8644, endothelin peptides, or platelet-activating factor.
  • Responses to U-46619 recovered to 50% of control within 90 minutes, indicating reversibility.
  • Responses to arachidonic acid were significantly decreased post-daltroban administration.

Conclusions:

  • Daltroban selectively and competitively antagonizes TxA2-receptor-mediated responses in the feline pulmonary vasculature.
  • The findings support the existence of discrete TxA2 receptors, separate from those activated by PGF2α, PGD2, or 9α,11β-PGF2.
  • Pulmonary vasoconstriction induced by platelet-activating factor and endothelin peptides is not mediated via TxA2 receptor activation in cats.

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