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首页> 外文期刊>Brain research bulletin >Effects of angiotensin type 2 receptor on secretion of the locus coeruleus in stress-induced hypertension rats
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Effects of angiotensin type 2 receptor on secretion of the locus coeruleus in stress-induced hypertension rats

机译：血管紧张素2型受体对应激性高血压大鼠血浆蓝藻分泌的影响

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Locus coeruleus (LC) has noradrenergic nerve terminals projecting to hypothalamus that modulating cardiovascular activity. To study the dynamic characteristics of norepinephrine (NE) release in hypothalamus followed by electrical stimulation in the locus coeruleus in the stress-induced hypertension (SIH) rats, we established the hypertension model rats by stimulations combining noise and foot-shock stress. After the end of modeling, NE release in the hypothalamus by electrical stimulation in LC was studied and NE signal was recorded by carbon fiber electrode. The peak value, the time to peak and half-life period of NE signal in both group rats were analyzed. Furthermore, to clarify the role of angiotensin II type 2 receptors (AT(2)) in norepinephrine (NE) release and the blood pressure of rat model of stress-induced hypertension, we intraperitoneally administered the AT(2) receptor antagonist PD123319 (AT(2) receptor antagonist, 0.3 mg/kg, i.p.) and intracerebroventricularly injection of CGP42112 (AT(2) receptor agonist, 6 mu g/5 mu l, i.c.v.) to adult male rats. We found the peak value of NE signal in the hypothalamus followed by electrical stimulation in the LC in SIH rats were higher than that in controls (P<0.01). Intraperitoneal injection of PD123319 (AT(2) receptor antagonist) potentiated electrical stimulation in the LC induced NE release in the hypothalamus in SIH rats and elevated blood pressure (P<0.05), whereas intracerebroventricular injection of CGP42112 (AT(2) receptor agonist) inhibited the NE release and reduced the heart rate (P<0.05). These results suggest that combining noise and foot-shock stresses increased the blood pressure and the secretion of NE in the hypothalamus followed by electrical stimulation in the LC in rats. AT2 receptors can inhibit the secretion of NE from the LC to the hypothalamus. The attenuation of presynaptic action of AT(2) receptor may play a role in the pathophysiological mechanism of SIH in rats. (C) 2014 Elsevier Inc. All rights reserved.
机译：蓝斑轨迹（LC）的去甲肾上腺素能神经末梢投射到下丘脑，从而调节心血管活动。为了研究应激性高血压（SIH）大鼠下丘脑中去甲肾上腺素（NE）释放，然后在电刺激蓝斑中电刺激的动态特征，我们建立了噪声和足底冲击刺激相结合的高血压模型大鼠。建模结束后，研究了LC电刺激下丘脑中NE的释放，并通过碳纤维电极记录NE信号。分析两组大鼠NE信号的峰值，到达峰值的时间和半衰期。此外，为了阐明血管紧张素II 2型受体（AT（2））在去甲肾上腺素（NE）释放和血压诱发的高血压大鼠模型中的作用，我们腹膜内给予AT（2）受体拮抗剂PD123319（AT （2）受体拮抗剂0.3 mg / kg，腹腔注射）并向成年雄性大鼠脑室内注射CGP42112（AT（2）受体激动剂，6μg/ 5μl，icv）。我们发现SIH大鼠下丘脑中NE信号的峰值以及电刺激下LC的峰值高于对照组（P <0.01）。腹膜内注射PD123319（AT（2）受体拮抗剂）增强了LC的电刺激，导致SIH大鼠下丘脑NE释放并血压升高（P <0.05），而脑室内注射CGP42112（AT（2）受体激动剂）抑制NE释放并降低心率（P <0.05）。这些结果表明，噪声和足部冲击的结合增加了大鼠下丘脑的血压和NE的分泌，继之以LC电刺激大鼠。 AT2受体可以抑制NE从LC到下丘脑的分泌。 AT（2）受体突触前作用的减弱可能在大鼠SIH的病理生理机制中起作用。 （C）2014 Elsevier Inc.保留所有权利。

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