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首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Stimulation of angiotensin type 1A receptors on catecholaminergic cells contributes to angiotensin-dependent hypertension
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Stimulation of angiotensin type 1A receptors on catecholaminergic cells contributes to angiotensin-dependent hypertension

机译：儿茶酚胺能细胞上血管紧张素1A型受体的刺激导致血管紧张素依赖性高血压

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摘要

Hypertension contributes to multiple forms of cardiovascular disease and thus morbidity and mortality. The mechanisms inducing hypertension remain unclear although the involvement of homeostatic systems, such as the renin-angiotensin and sympathetic nervous systems, is established. A pivotal role of the angiotensin type 1 receptor in the proximal tubule of the kidney for the development of experimental hypertension is established. Yet, other systems are involved. This study tests whether the expression of angiotensin type 1A receptors in catecholaminergic cells contributes to hypertension development. Using a Cre-lox approach, we deleted the angiotensin type 1A receptor from all catecholaminergic cells. This deletion did not alter basal metabolism or blood pressure but delayed the onset of angiotensin-dependent hypertension and reduced the maximal response. Cardiac hypertrophy was also reduced. The knockout mice showed attenuated activation of the sympathetic nervous system during angiotensin II infusion as measured by spectral analysis of the blood pressure. Increased reactive oxygen species production was observed in forebrain regions, including the subfornical organ, of the knockout mouse but was markedly reduced in the rostral ventrolateral medulla. These studies demonstrate that stimulation of the angiotensin type 1A receptor on catecholaminergic cells is required for the full development of angiotensin-dependent hypertension and support an important role for the sympathetic nervous system in this model.
机译：高血压会导致多种形式的心血管疾病，进而导致发病率和死亡率。尽管建立了体内稳态系统，例如肾素-血管紧张素和交感神经系统，但诱发高血压的机制仍不清楚。建立了1型血管紧张素受体在肾脏近端小管中对于实验性高血压发展的关键作用。但是，还涉及其他系统。这项研究测试了儿茶酚胺能细胞中血管紧张素1A型受体的表达是否有助于高血压的发展。使用Cre-lox方法，我们从所有儿茶酚胺能性细胞中删除了1A型血管紧张素受体。这种删除并没有改变基础代谢或血压，但延迟了血管紧张素依赖性高血压的发作并降低了最大反应。心脏肥大也减少了。基因敲除小鼠显示在血管紧张素II输注过程中交感神经系统的激活减弱，这是通过对血压的频谱分析测得的。观察到在敲除小鼠的前脑区域，包括子下器官中，活性氧的产生增加，但在前额腹外侧延髓中明显减少。这些研究表明，充分发展血管紧张素依赖性高血压需要刺激儿茶酚胺能细胞上的血管紧张素1A受体，并且在该模型中支持交感神经系统的重要作用。

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