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Selective estrogen receptor-alpha and estrogen receptor-beta agonists rapidly decrease pulmonary artery

Tim Lahm1, Paul R Crisostomo, Troy A Markel

  • 1Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana, USA.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|October 4, 2008
PubMed
Summary
This summary is machine-generated.

Estrogen receptors alpha and beta rapidly decrease pulmonary artery vasoconstriction through nitric oxide-dependent pathways. ER-alpha affects phenylephrine responses, while ER-beta influences hypoxic vasoconstriction, indicating stimulus-specific roles.

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Area of Science:

  • Cardiovascular Physiology
  • Endocrinology
  • Pulmonary Medicine

Background:

  • Estrogen is known to reduce pulmonary artery (PA) vasoconstriction.
  • The specific roles of estrogen receptor (ER)-alpha and ER-beta, and their stimulus-dependency, in this process are unclear.

Purpose of the Study:

  • To investigate whether selective ER-alpha and ER-beta agonists rapidly decrease PA vasoconstriction.
  • To determine if these effects are mediated by nitric oxide (NO) and are stimulus-dependent.

Main Methods:

  • Utilized isolated rat PA rings in organ baths to measure vasoconstriction and vasorelaxation.
  • Administered selective ER-alpha (propylpyrazole triol, PPT) and ER-beta (diarylpropiolnitrile, DPN) agonists.
  • Assessed responses to phenylephrine and hypoxia, with and without the NO-synthase inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME).

Main Results:

  • Selective ER-alpha activation (PPT) rapidly decreased phenylephrine-induced vasoconstriction and enhanced endothelium-dependent vasorelaxation, effects blocked by l-NAME.
  • Selective ER-beta activation (DPN) rapidly decreased hypoxic pulmonary vasoconstriction (HPV), an effect also abolished by l-NAME.
  • Lower agonist concentrations were less effective, and immediate effects suggested nongenomic mechanisms.

Conclusions:

  • Both ER-alpha and ER-beta contribute to decreasing PA vasoconstriction via NO-dependent mechanisms.
  • ER-alpha primarily modulates phenylephrine-induced vasoconstriction, while ER-beta inhibits HPV.
  • The stimulus-specific actions of ERs highlight distinct roles in regulating pulmonary vascular tone.