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首页> 外文期刊>Life sciences >In vivo effects of partial phosphorothioated AT1 receptor antisense oligonucleotides in spontaneously hypertensive and normotensive rats.
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In vivo effects of partial phosphorothioated AT1 receptor antisense oligonucleotides in spontaneously hypertensive and normotensive rats.

机译：自发性高血压和血压正常大鼠中部分硫代磷酸化AT1受体反义寡核苷酸的体内作用。

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摘要

Partial phosphorothioate (PS) antisense oligodeoxynucleotides (ODNs) targeted against rat AT1 receptor mRNA have been used to control blood pressure in normotensive (WKY) and spontaneously hypertensive (SHR) rats. Molecules were injected intracerebroventricularly (i.c.v., right lateral ventricle) in freely moving animals. The antisense ODN lowered the mean arterial pressure (MAP) 24 hours (-43 mmHg+/-10) and 48 hours (-30 mmHg+/-13) after injection, while the control ODN molecule had no significant effects. The observed decrease of blood pressure was due to a specific inhibition of AT1 receptor gene expression, since the level of its mRNA, monitored by reverse transcription (RT)- polymerase chain reaction (PCR), was significantly reduced by antisense molecule (-40%), compared to sense one. In normotensive rats no effect on MAP have been observed, while AT1 receptor gene expression is reduced (-40%) by antisense treatment. It is known that SHRs have an enhanced basal activity of the central renin-angiotensin system that induces an increase in central sympathetic outflow. Instead in WKY rats the central sympathetic outflow is not conditioned by the enhanced activity of brain renin-angiotensin system. Therefore in normotensive rats although partial PS ODN reduces the AT1 mRNA level this will not result in a modification of the sympathetic outflow and no change in MAP level would be observed.
机译：靶向大鼠AT1受体mRNA的部分硫代磷酸酯（PS）反义寡聚脱氧核苷酸（ODN）已被用于控制血压正常（WKY）和自发性高血压（SHR）大鼠的血压。将脑室内（i.c.v.，右侧脑室）注射到自由运动的动物体内。注射后24小时（-43 mmHg +/- 10）和48小时（-30 mmHg +/- 13），反义ODN降低了平均动脉压（MAP），而对照ODN分子则无明显作用。观察到的血压降低归因于对AT1受体基因表达的特异性抑制，因为通过反转录（RT）-聚合酶链反应（PCR）监测的其mRNA水平被反义分子显着降低（-40％ ），相比之下感官之一。在血压正常的大鼠中，未观察到对MAP的影响，而通过反义处理，AT1受体基因的表达降低了（-40％）。众所周知，SHR具有增强的中央肾素-血管紧张素系统基础活性，从而导致中央交感神经外流增加。相反，在WKY大鼠中，中央交感神经外流不受脑肾素-血管紧张素系统活性增强的调节。因此，在血压正常的大鼠中，尽管部分PS ODN会降低AT1 mRNA的水平，但这不会导致交感神经流出的改变，并且不会观察到MAP水平的变化。

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