Estrogen enhancement of baroreflex sensitivity is centrally mediated
Estrogen enhancement of baroreflex sensitivity is centrally mediated
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DOI：
10.1152/ajpregu.1999.276.4.r1030
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发表时间：
1999-04-01
影响因子：
2.8
通讯作者：
Abdel-Rahman, AA
中科院分区：
文献类型：
--
作者：
Mohamed, MK;El-Mas, MM;Abdel-Rahman, AA
我们最近发现，雌激素可以增强清醒大鼠压力感受器对反射性心动过缓的控制。目前的研究在戊巴比妥钠麻醉的大鼠中复制了这一发现，并且该研究被扩展以调查雌激素的这种作用是中枢介导的还是外周介导的。在戊巴比妥钠麻醉的假手术 (SO)、卵巢切除 (OVX) 和 OVX 雌二醇处理的 Sprague-Dawley 大鼠中评估主动脉降压肌中央端或迷走神经传出神经电刺激的血流动力学反应。去氧肾上腺素（1-16 μg/kg iv）引起剂量依赖性的加压和心动过缓反应。与平均动脉压和心率变化相关的压力反射曲线的回归分析显示，与SO麻醉大鼠相比，OVX的压力反射敏感性显着较小（分别为-0.54 +/- 0.05和-0.91 +/- 0.12beats.min(-1).mmHg(-1)；P < 0.05）。用17β-雌二醇（E-2，50μg.kg(-1).day(-1)，皮下注射2天）治疗OVX大鼠，压力反射敏感性显着增强，达到与SO大鼠相似的水平（P < 0.05）。在清醒和麻醉的大鼠中观察到，E-2 对压力感受反射介导的心动过缓的增强作用似乎是选择性的，因为在另一组清醒大鼠中测量的压力感受反射介导的心动过速反应并未因卵巢切除或 Ea 给药而改变。电刺激主动脉神经引起频率依赖性降压和心动过缓反应，与 SO 值相比，OVX 中的反应明显较小（P < 0.05）。用 E-2 治疗 OVX 大鼠，使主动脉刺激的血流动力学反应恢复到接近 SO 水平。另一方面，迷走神经刺激的血流动力学反应不受 OVX 或 E-2 治疗的影响。这些发现表明，雌激素对反射性心动过缓的增强是中枢介导的，并且涉及与主动脉神经的中央投射的相互作用。
We have recently shown that estrogen enhances baroreceptor control of reflex bradycardia in conscious rats. The present study replicated this finding in pentobarbital sodium-anesthetized rats, and the study was extended to investigate whether this effect of estrogen is centrally or peripherally mediated. Hemodynamic responses to electrical stimulation of the central end of the aortic depressor or the vagal efferent nerve were evaluated in pentobarbital sodium-anesthetized sham-operated (SO), ovariectomized (OVX), and OVX estradiol-treated Sprague-Dawley rats. Phenylephrine (1-16 mu g/kg iv) elicited dose-dependent presser and bradycardic responses. Regression analysis of the baroreflex curves, relating changes in mean arterial pressure and heart rate, revealed a significantly smaller baroreflex sensitivity in OVX compared with SO anesthetized rats (-0.54 +/- 0.05 and -0.91 +/- 0.12 beats.min(-1).mmHg(-1), respectively; P < 0.05). Treatment of OVX rats with 17 beta-estradiol (E-2, 50 mu g.kg(-1).day(-1) for 2 days subcutaneously) significantly enhanced baroreflex sensitivity to a level similar to that of SO rats (P < 0.05). The enhancing effect of E-2 on the baroreflex-mediated bradycardia, observed in conscious and anesthetized rats, seems to be selective because the baroreflex-mediated tachycardic responses measured in a separate group of conscious rats were not altered by ovariectomy or Ea administration. Electrical stimulation of the aortic nerve elicited frequency-dependent depressor and bradycardic responses that were significantly smaller in OVX compared with SO values (P < 0.05). Treatment of OVX rats with E-2 restored the hemodynamic responses to aortic stimulation to near SO levels. On the other hand, hemodynamic responses to vagal stimulation were not affected by OVX or treatment with E-2. These findings suggest that enhancement of reflex bradycardia by estrogen is centrally mediated and involves interaction with central projections of the aortic nerve.