FULMINANT HYPERTENSION IN TRANSGENIC RATS HARBORING THE MOUSE REN-2 GENE
FULMINANT HYPERTENSION IN TRANSGENIC RATS HARBORING THE MOUSE REN-2 GENE
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DOI：
10.1038/344541a0
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发表时间：
1990-04-05
期刊：
影响因子：
64.8
通讯作者：
GANTEN, D
中科院分区：
文献类型：
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作者：
MULLINS, JJ;PETERS, J;GANTEN, D
原发性高血压是一种多基因疾病，血压异常升高。它仍然是心血管疾病以及脑出血、心力衰竭和肾脏疾病导致死亡的主要原因。几种参与血压稳态的蛋白质的基因已被克隆和表征1-8，包括肾素-血管紧张素系统的基因，该系统在血压控制中发挥核心作用9-10。在这里，我们描述了将小鼠Ren-2肾素基因3,11-13引入大鼠基因组中，并证明该基因的表达会导致严重高血压。这些转基因动物代表了高血压的模型，其中该疾病的遗传基础是已知的。此外，由于转基因动物在肾脏中不会过度表达活性肾素，并且血浆中的活性肾素水平较低，因此它们还提供了低肾素高血压的新模型。
PRIMARY hypertension is a polygenic condition in which blood pressure is enigmatically elevated; it remains a leading cause of cardiovascular disease and death due to cerebral haemorrhage, cardiac failure and kidney disease. The genes for several of the proteins involved in blood pressure homeostasis have been cloned and characterized1–8, including those of the renin–angiotensin system, which plays a central part in blood pressure control9–10. Here we describe the introduction of the mouseRen-2renin gene3,11–13into the genome of the rat and demonstrate that expression of this gene causes severe hypertension. These trans-genic animals represent a model for hypertension in which the genetic basis for the disease is known. Further, as the transgenic animals do not overexpress active renin in the kidney and have low levels of active renin in their plasma, they also provide a new model for low-renin hypertension.