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首页> 外文期刊>American Journal of Physiology >Central angiotensin II-induced pressor responses and neural activity in utero and hypothalamic angiotensin receptors in preterm ovine fetus.
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Central angiotensin II-induced pressor responses and neural activity in utero and hypothalamic angiotensin receptors in preterm ovine fetus.

机译：中枢血管紧张素II诱导早产儿胎儿子宫和下丘脑血管紧张素受体的升压反应和神经活动。

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The central renin-angiotensin system is important in the control of blood pressure in the adult. However, few data exist about the in utero development of central angiotensin-mediated pressor responses. Our recent studies have shown that the application of ANG II into the fetal brain can increase blood pressure at near term. The present study determined fetal blood pressure and heart rate in response to a central application of ANG II in the chronically prepared preterm ovine fetus, determined the action sites marked by c-Fos expression in the fetal central pathways after intracerebroventricular injection of ANG II in utero, and determined angiotensin subtype 1 receptors in the fetal hypothalamus. Central injection of ANG II significantly increased fetal mean arterial pressure (MAP). Adjusted fetal MAP against amniotic pressure was also increased by ANG II. Fetal heart rate was subsequently decreased after the central administration of ANG II and/or the increase of blood pressure. ANG II induced c-Fos expression in the central putative cardiovascular area, the paraventricular nuclei in the brain sympathetic pathway. Application of ANG II also caused intense Fos immunoreactivity in the tractus solitarius nuclei in the hindbrain. In addition, intense angiotensin subtype 1 receptors were expressed in the hypothalamus at preterm. These data demonstrate that central ANG II-related pressor centers start to function as early as at preterm and suggest that the central angiotensin-related sympathetic pathway is likely intact in the control of blood pressure in utero.
机译：中央肾素-血管紧张素系统在成年人的血压控制中很重要。但是，很少有关于子宫中枢血管紧张素介导的升压反应发育的数据。我们最近的研究表明，在胎儿脑中应用ANG II可以在短期内增加血压。本研究确定了在长期准备的早产胎儿中对ANG II的中枢应用的响应的胎儿血压和心率，确定了在脑室内向子宫内注射ANG II后胎儿中枢通路中c-Fos表达标记的作用位点，并确定胎儿下丘脑中的血管紧张素亚型1受体。 ANG II的中央注射显着增加了胎儿平均动脉压（MAP）。 ANG II也增加了针对羊水的调整胎儿MAP。继用ANG II和/或血压升高后，胎儿心率随后下降。 ANG II诱导c-Fos在中央推测的心血管区域，即脑交感神经通路的室旁核中表达。 ANG II的应用还引起后脑孤束核强烈的Fos免疫反应性。另外，早产时下丘脑中表达强烈的血管紧张素亚型1受体。这些数据表明，中枢ANG II相关的升压中心早在早产时就开始起作用，并表明中枢血管紧张素相关的交感途径可能在子宫内血压控制中完好无损。

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