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

Micromolar concentrations of the biologically active oestrogen 17 beta-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 (ER beta) for oestrogen-induced vascular relaxation. 17 beta-oestradiol was added to aortic rings from ER beta knock-out (-/-) and wild-type (+/+) mice precontracted with noradrenaline, 17 beta-oestradiol caused a concentration-dependent (1-100 mu M) relaxation of aortic rings from both -/- and +/+ animals of both sexes. Rings from male and female -/- mice were more sensitive to 17 beta-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 ER beta modulates vascular relaxation to mu M concentrations of oestrogen; lack of ER beta renders the vascular wall supersensitive to 17 beta-oestradiol. Lack of ER beta caused no change in vascular wall morphology suggesting that this ER subtype is not involved in vascular structure development.