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β-雌二醇对去氧肾上腺素和血管紧张素II所致收缩的主动脉环的体外舒张作用

In vitro relaxation of phenylephrine- and angiotensin II-contracted aortic rings by beta-estradiol.

作者信息

Ravi J, Mantzoros C S, Prabhu A S, Ram J L, Sowers J R

机构信息

Division of Endocrinology and Hypertension, Wayne State University, Detroit, Michigan 48201.

出版信息

Am J Hypertens. 1994 Dec;7(12):1065-9. doi: 10.1093/ajh/7.12.1065.

Abstract

In vivo studies suggest that 17 beta-estradiol (beta E) may regulate vascular tone. Results of recent studies suggest that beta E exerts rapid effects on intracellular calcium, possibly via cell surface receptors, distinct from conventional nuclear receptors for steroids. The present study was designed to determine whether beta E acutely modifies vascular smooth muscle contractile responses to phenylephrine (PE) and angiotensin II (AII). In experiments on tonic responses of aortic rings to 5 x 10(-8) mol/L PE, cumulative additions of beta E reduced tension at concentrations > 10(-6) mol/L. Contractile dose responses to PE were determined in rat aortic rings in absence of sex hormones and then after exposure to beta E (5 x 10(-6) mol/L, n = 6) or vehicle (ETOH, n = 6) for 30 min. beta E increased ED50 and reduced maximal responses. Application of 5 x 10(-6) mol/L beta E for 30 min also reduced the contractile response to 1 mmol/L AII from 69 +/- 4% (vehicle) to 47 +/- 6% (estradiol) of maximal KCl contraction (P < .025, n = 7). These data suggest that beta E acutely attenuates vasoconstrictor responses to PE as well as to AII, possibly by an effect exerted at the cell membrane level.

摘要

体内研究表明,17β-雌二醇(βE)可能调节血管张力。近期研究结果表明,βE可能通过细胞表面受体对细胞内钙产生快速影响,这与传统的类固醇核受体不同。本研究旨在确定βE是否能急性改变血管平滑肌对去氧肾上腺素(PE)和血管紧张素II(AII)的收缩反应。在主动脉环对5×10⁻⁸mol/L PE的张力反应实验中,当βE浓度>10⁻⁶mol/L时,累积添加βE可降低张力。在不存在性激素的情况下,然后在暴露于βE(5×10⁻⁶mol/L,n = 6)或溶剂(乙醇,n = 6)30分钟后,测定大鼠主动脉环对PE的收缩剂量反应。βE增加了半数有效剂量(ED50)并降低了最大反应。应用5×10⁻⁶mol/L βE 30分钟也将对1mmol/L AII的收缩反应从最大氯化钾收缩的69±4%(溶剂)降低至47±6%(雌二醇)(P <.025,n = 7)。这些数据表明,βE可能通过在细胞膜水平发挥作用,急性减弱血管对PE以及AII的收缩反应。

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