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Renal c-fos expression induced by angiotensin II is enhanced in spontaneously hypertensive rats.

机译:在自发性高血压大鼠中,由血管紧张素II诱导的肾脏c-fos表达增强。

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摘要

We compared the effect of a bolus injection of angiotensin II (Ang II) on the expression of protooncogene c-fos in the renal cortex and medulla of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Intravenous infusion of 5 ng/kg body weight of Ang II resulted in an immediate rise in systolic blood pressure (SBP) in both SHR and WKY rats. The percent rise in SBP was similar in both strains. Pretreatment with Ang II type 1 (AT1)-receptor antagonist, L-158,809 (1 mg/kg) abolished the pressor response in both strains. Competitive reverse transcription-polymerase chain reaction (RT-PCR) showed that administration of Ang II increased the expression of c-fos mRNA within 10 min in both the renal cortex and medulla of SHR significantly higher than WKY rats. Moreover, the enhanced c-fos mRNA expression due to Ang II was significantly suppressed by the pretreatment of L-158,809 in both strains. These findings indicate that c-fos expression in the kidney is mediated by AT1-receptors and that the renal c-fos response to exogenous Ang II was significantly augmented in SHR compared with WKY rats, suggesting that this hyperresponsiveness on renal AT1-action may partly contribute to the progression of renal injury in SHR.
机译:我们比较了大剂量注射血管紧张素II(Ang II)对自发性高血压大鼠(SHR)和Wistar-Kyoto(WKY)大鼠肾皮质和髓质中原癌基因c-fos表达的影响。静脉输注5 ng / kg体重的Ang II导致SHR和WKY大鼠的收缩压(SBP)立即升高。两种菌株的SBP上升百分比相似。用Ang II 1型(AT1)受体拮抗剂L-158,809(1 mg / kg)进行的预处理均消除了两种菌株的升压反应。竞争性逆转录-聚合酶链反应(RT-PCR)显示,Ang II的施用在10分钟内增加了SHR肾皮质和髓质中c-fos mRNA的表达,明显高于WKY大鼠。此外,在两种菌株中,L-158,809的预处理均显着抑制了由于Ang II引起的c-fos mRNA表达的增强。这些发现表明,肾脏中的c-fos表达是由AT1受体介导的,并且与WKY大鼠相比,SHR对肾脏对外源性Ang II的c-fos反应显着增强,表明这种对肾脏AT1作用的高反应性可能部分有助于SHR中肾损伤的进展。

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