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Increased magnitude of relaxation to oestrogen in aorta from oestrogen receptor beta knock-out mice

In English

Författare

Summary, in English

Micromolar concentrations of the biologically active oestrogen 17beta-oestradiol reduce agonist-induced force in vascular preparations through an unidentified mechanism. The aim of the present study was to investigate the importance of oestrogen receptor beta (ERbeta) for oestrogen-induced vascular relaxation. 17beta-oestradiol was added to aortic rings from ERbeta knock-out (-/-) and wild-type (+/+) mice precontracted with noradrenaline. 17beta-oestradiol caused a concentration-dependent (1-100 microM) relaxation of aortic rings from both -/- and +/+ animals of both sexes. Rings from male and female -/- mice were more sensitive to 17beta-oestradiol than those from +/+ mice. Medial thickness, determined by computerized image analysis, was similar in rings from -/- and +/+ animals. Endothelium, as determined by immuno-cytochemistry, was present in -/- and +/+ aorta. Maximal noradrenaline evoked force and sensitivity to noradrenaline were similar in both groups. In summary ERbeta modulates vascular relaxation to microM concentrations of oestrogen; lack of ERbeta renders the vascular wall supersensitive to 17beta-oestradiol. Lack of ERbeta caused no change in vascular wall morphology suggesting that this ER subtype is not involved in vascular structure development.

Publiceringsår

2000-08

Språk

Engelska

Sidor

5-9

Publikation/Tidskrift/Serie

Journal of Endocrinology

Volym

166

Issue

2

Dokumenttyp

Artikel i tidskrift

Förlag

Society for Endocrinology

Ämne

  • Physiology

Nyckelord

  • Animals
  • Aorta
  • Body Weight
  • Dose-Response Relationship, Drug
  • Endothelium, Vascular
  • Estradiol
  • Estrogen Receptor beta
  • Female
  • Image Processing, Computer-Assisted
  • Immunohistochemistry
  • In Vitro Techniques
  • Male
  • Mice
  • Mice, Knockout
  • Microscopy, Fluorescence
  • Muscle, Smooth, Vascular
  • Norepinephrine
  • Receptors, Estrogen
  • Vasoconstriction

Status

Published

ISBN/ISSN/Övrigt

  • ISSN: 0022-0795