Effect of acute and long-term treatment with 17-β-estradiol on the vasomotor responses in the rat aorta

摘要

class="enumerated" style="list-style-type:decimal">This study sought to evaluate whether the effects of acute and long-term treatment with 17-β-estradiol on the vasomotor responses in rat aortic rings are mediated through the same mechanism.Ovariectomized rats were treated daily with either 17-β-estradiol-3-benzoate (100 μg kg⁻¹) or vehicle for 1 week.The effect of long-term 17-β-estradiol treatment on the responses to cumulative doses of phenylephrine, 5-HT, calcium, potassium and 17-β-estradiol was determined in aortic rings. In the same rings, the effect of acute exposure to 17-β-estradiol (5 and 10 μM) on the dose response curves for phenylephrine, 5-HT, calcium, potassium and acetylcholine were estimated. The measurements were made in rings with and without intact endothelium. The tone-related basal release of nitric oxide (NO) was measured in rings with intact endothelium.Long-term 17-β-estradiol treatment reduced the maximum developed contraction to all contracting agents studied. This effect was abolished in endothelium denuded vessels. Acute 17-β-estradiol treatment also reduced maximal contraction. This effect, however, was independent of the endothelium.Long-term 17-β-estradiol treatment significantly increased the ability of the rings to dilate in response to acetylcholine whereas acute exposure to 17-β-estradiol had no effect. The tone-related release of NO was significantly increased after long-term exposure to 17-β-estradiol.In conclusion, this study indicate that the acute and long-term effects of 17-β-estradiol in the rat aorta are mediated through different mechanisms. The long-term effect is mediated through the endothelium most likely by increasing NO release. In contrast, the acute effect of 17-β-estradiol seems to be through an effect on the vascular smooth muscle cells.