首页> 外文期刊>American Journal of Physiology >Central angiotensin II AT1 receptors mediate fetal swallowing and pressor responses in the near-term ovine fetus.
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Central angiotensin II AT1 receptors mediate fetal swallowing and pressor responses in the near-term ovine fetus.

机译:中枢血管紧张素II AT1受体介导近期绵羊胎儿的吞咽和升压反应。

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Swallowed volumes in the fetus are greater than adult values (per body weight) and serve to regulate amniotic fluid volume. Central ANG II stimulates swallowing, and nonspecific ANG II receptor antagonists inhibit both spontaneous and ANG II-stimulated swallowing. In the adult rat, AT1 receptors mediate both stimulated drinking and pressor activities, while the role of AT2 receptors is controversial. As fetal brain contains increased ANG II receptors compared with the adult brain, we sought to investigate the role of both AT1 and AT2 receptors in mediating fetal swallowing and pressor activities. Five pregnant ewes with singleton fetuses (130 +/- 1 days) were prepared with fetal vascular and lateral ventricle (LV) catheters and electrocorticogram and esophageal electromyogram electrodes and received three studies over 5 days. On day 1 (ANG II), following a 2-h basal period, 1 ml artificial cerebrospinal fluid (aCSF) was injected in the LV. At time 4 h, ANG II (6.4 microg) was injected in the LV, and the fetus was monitored for a final 2 h. On day 3, AT1 receptor blocker (losartan 0.5 mg) was administered at 2 h, and ANG II plus losartan was administered at 4 h. On day 5, AT2 receptor blocker (PD-123319; 0.8 mg was administered at 2 h and ANG II plus PD-123319 at 4 h. In the ANG II study, LV injection of ANG II significantly increased fetal swallowing (0.9 +/- 0.1 to 1.4 +/- 0.1 swallows/min; P < 0.05). In the losartan study, basal fetal swallowing significantly decreased in response to blockade of AT1 receptors (0.9 +/- 0.1 to 0.4 +/- 0.1 swallows/min; P < 0.05), while central injection of ANG II in the presence of AT1 receptor antagonism did not increase fetal swallowing (0.6 +/- 0.1 swallows/min). In the PD-123319 study, basal fetal swallowing did not change in response to blockade of AT2 receptor (0.9 +/- 0.1 swallows/min), while central injection of ANG II in the presence of AT2 blockade significantly increased fetal swallowing (1.5 +/- 0.1 swallows/min; P < 0.05). ANG II caused significant pressor responses in the control and PD-123319 studies but no pressor response in the presence of AT1 blockade. These data demonstrate that in the near-term ovine fetus, AT1 receptor but not AT2 receptors accessible via CSF contribute to dipsogenic and pressor responses.
机译:胎儿的吞咽量大于成人值(每体重),可用来调节羊水量。中枢ANG II刺激吞咽,非特异性ANG II受体拮抗剂抑制自发吞咽和ANG II刺激的吞咽。在成年大鼠中,AT1受体介导刺激的饮酒和升压活动,而AT2受体的作用是有争议的。由于与成人大脑相比,胎儿大脑中ANG II受体的含量增加,我们试图研究AT1和AT2受体在介导胎儿吞咽和升压活动中的作用。使用胎儿血管和侧脑室(LV)导管以及脑电图和食管肌电图电极准备了五只单胎胎儿妊娠母羊(130 +/- 1天),并在5天内接受了三项研究。在第2天的基础期后第1天(ANG II),将1 ml人工脑脊髓液(aCSF)注入左室。在4小时的时间,将ANG II(6.4微克)注射到LV中,并在最后2小时监测胎儿。在第3天,在2小时时施用AT1受体阻滞剂(氯沙坦0.5mg),并在4小时时施用ANG II加氯沙坦。在第5天,AT2受体阻滞剂(PD-123319;在2 h时施用0.8 mg,在ANG II和PD-123319在4 h时施用。在ANG II研究中,LV注射ANG II显着增加了胎儿吞咽(0.9 +/- 0.1至1.4 +/- 0.1吞咽/分钟; P <0.05)在氯沙坦研究中,基础胎儿吞咽对AT1受体的阻滞反应明显降低(0.9 +/- 0.1至0.4 +/- 0.1吞咽/分钟; P <0.05),而在AT1受体拮抗作用下集中注射ANG II不会增加胎儿吞咽(0.6 +/- 0.1吞咽/分钟)。在PD-123319研究中,基础吞咽并没有因阻断而改变AT2受体的吞咽(0.9 +/- 0.1吞咽/分钟),而在存在AT2阻滞的情况下集中注射ANG II则显着增加了胎儿吞咽(1.5 +/- 0.1吞咽/分钟; P <0.05)。对照研究和PD-123319研究显示,在AT1阻滞存在时无升压反应,这些数据表明r-term绵羊胎儿,AT1受体而不是可通过CSF进入的AT2受体,会导致血沉和升压反应。

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