| First Author | Nilsson BO | Year | 2000 |
| Journal | J Endocrinol | Volume | 166 |
| Issue | 2 | Pages | R5-9 |
| PubMed ID | 10927637 | Mgi Jnum | J:64165 |
| Mgi Id | MGI:1888817 | Doi | 10.1677/joe.0.166r005 |
| Citation | Nilsson BO, et al. (2000) Increased magnitude of relaxation to oestrogen in aorta from oestrogen receptor beta knock-out mice. J Endocrinol 166(2):R5-9 |
| abstractText | 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. |
