Effects of estrogen replacement on stress-induced cardiovascular responses via renin-angiotensin system in ovariectomized rats.
Effects of estrogen replacement on stress-induced cardiovascular responses via renin-angiotensin system in ovariectomized rats.
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雌激素替代对去势大鼠肾素-血管紧张素系统应激诱导的心血管反应的影响。
DOI：
10.1152/ajpregu.00415.2015
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Morimoto K
中科院分区：
文献类型：
--
作者：
Tazumi S;Yokota N;Kawakami M;Omoto S;Takamata A;Morimoto K
本研究的目的是确定卵巢切除大鼠的长期雌激素替代是否通过减弱肾素-血管紧张素系统的激活来抑制对心理压力的升压反应。 9周龄雌性Wistar大鼠被切除卵巢。 4周后，大鼠被随机分配皮下植入含有17β-雌二醇（E2）或安慰剂（Pla）的颗粒。治疗 4 周后，大鼠经历了笼子转换应激，在一项单独的实验中，一部分大鼠接受了血管紧张素 II 的输注。通过无线电遥测技术测量，两组的血压（BP）和心率（HR）迅速升高。然而，与 Pla 组相比，E2 组的血压和心率对压力的反应显着减弱。一种血管紧张素 II 1 型受体阻滞剂氯沙坦通过饮用水给药，消除了两组之间对压力的升压反应的差异。此外，应激引起的血浆肾素活性和血管紧张素II浓度升高在Pla组中显着，但在E2组中则不显着。此外，E2组肾脏中肾素mRNA的表达相对于Pla组较低。最后，我们发现静脉输注血管紧张素 II 在两组中的血压升高和心率降低的程度相似。这些结果表明，雌激素对心理应激引起的肾素-血管紧张素系统激活的抑制作用可能至少部分原因是在雌激素替代的卵巢切除大鼠中观察到的对心理应激的升压反应的抑制。
The purpose of this study was to determine whether chronic estrogen replacement in ovariectomized rats inhibits the pressor response to psychological stress by attenuating the activation of the renin-angiotensin system. Female Wistar rats aged 9 wk were ovariectomized. After 4 wk, the rats were randomly assigned to be implanted subcutaneously with pellets containing either 17β-estradiol (E2) or placebo (Pla). After 4 wk of treatment, the rats underwent cage-switch stress and, in a separate experiment, a subset received an infusion of angiotensin II. The cage-switch stress rapidly elevated blood pressure (BP) and heart rate (HR) as measured by radiotelemetry in both groups. However, the BP and HR responses to the stress were significantly attenuated in the E2 group compared with the Pla group. An angiotensin II type 1 receptor blocker, losartan, given in drinking water, abolished the difference in the pressor response to stress between the two groups. Moreover, the stress-induced elevation in plasma renin activity and angiotensin II concentration was significant in the Pla group, but not in the E2 group. In addition, the expression of renin mRNA in the kidney was lower in the E2 group relative to the Pla group. Finally, we found that intravenous angiotensin II infusion increased BP and decreased HR to a similar degree in both groups. These results suggest that the inhibitory effects of estrogen on psychological stress-induced activation of the renin-angiotensin system could be at least partially responsible for the suppression of the pressor responses to psychological stress seen in estrogen-replaced ovariectomized rats.