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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.
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The objective of this study was to investigate the effects of oestrogen receptor (ER) beta activation on vascular protein synthesis and protein expression. Nuclear immunoreactivity towards ER beta was observed abundantly in vascular smooth muscle and endothelial cells of mouse aorta. No ER alpha-positive cell nuclei were observed. In aorta from ovariectomized mice, treatment with the selective ER beta agonist genistein (100 nM) for 24 h increased [(3)H]leucine incorporation by about 30%. This effect was prevented by the ER blocker ICI 182780 (10 microM). Although genistein treatment stimulated protein synthesis, it caused no change in total protein determined either by the Lowry method on tissue homogenate or by densitometric scanning of protein bands (10-220 kDa) separated by SDS-PAGE. Separation of [(35)S]methionine-labelled proteins by SDS-PAGE did not reveal the protein(s) stimulated by genistein. DNA synthesis was not affected by 100 nM genistein, suggesting that genistein-induced stimulation of protein synthesis is not part of a growth response. Protein expression, determined by SDS-PAGE, was similar in aorta from ER beta-knockout and wild-type mice, suggesting that expression of vascular proteins does not depend solely on a functional ER beta gene. We suggest that activation of vascular ER beta stimulates synthesis of proteins and that this response is not associated with vascular growth.
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The role of oestrogen receptor (ER) beta in vascular function remains unclear. With the use of a specific ERbeta antibody we have now, using immunocytochemistry, visualized ERbeta in different parts of the vascular tree. In about 70% of medial smooth muscle cells of female rat aorta, tail artery and uterine artery, nuclear immunoreactivity to ERbeta was observed. In these vessels endothelial cells also expressed ERbeta. Vascular expression of the ERalpha subtype was lower than that of ERbeta. In aorta and tail artery, no immunoreactivity towards ERalpha was observed, while in uterine vessels occasional medial smooth muscle and endothelial cells expressed this ER subtype. ERbeta and alpha expression in uterine vessels was independent of the stage of the oestrous cycle, suggesting that variations in uterine blood flow occurring during the cycle are independent of ER density. The regional distribution of ERalpha, as determined by immunocytochemistry, was supported by measurements of ERalpha levels by enzyme immunoassay. In the uterine artery, the level of ERalpha was several times higher (P<0.001) than that of aorta and tail artery (10.1+/-1.7 fmol/mg protein in the uterine artery vs 3.3+/-1.0 and 0.5+/-0.5 fmol/mg protein in aorta and tail artery respectively). Thus, a prominent nuclear expression of ERbeta was observed in the vascular wall of several parts of the vascular tree, while ERalpha predominantly was expressed in uterine vessels, suggesting that ERbeta and alpha may have different roles in vascular function.
