Molecular mechanism of aggravation of hypertensive organ damages by short-term blood pressure variability.
Molecular mechanism of aggravation of hypertensive organ damages by short-term blood pressure variability.
复制标题
短期血压变异性加重高血压器官损害的分子机制。
DOI：
10.2174/1573402111666141217112655
复制
发表时间：
2014
影响因子：
2.3
通讯作者：
Imaizumi T
中科院分区：
文献类型：
--
作者：
Kai H;Kudo H;Takayama N;Yasuoka S;Aoki Y;Imaizumi T
越来越多的证据表明，不仅是收缩压和舒张压的升高，而且血压变异性(或波动性)的增加也与高血压器官损害和心脑血管事件的发病率和死亡率有关。然而，BP变异性增加加重高血压器官损害的分子机制仍不清楚。因此，我们通过对自发性高血压大鼠进行双侧窦-主动脉去神经手术，建立了一种高血压和大血压变异性相结合的慢性模型。我们使用该模型进行的一系列研究表明，大的血压变异性通过激活局部血管紧张素II和盐皮质激素受体系统而诱导慢性心肌炎症，从而加剧高血压心脏的心肌肥厚和心肌纤维化，导致收缩功能障碍。此外，大的血压变异性通过局部血管紧张素II系统导致高血压肾脏动脉硬化改变和缺血性皮质纤维化的加重。
There is increasing evidence that not only the elevation of systolic and diastolic blood pressure (BP) but also the increase in BP variability (or fluctuation) are associated with hypertensive organ damages and the morbidity and mortality of cerebrovascular and cardiovascular events. However, the molecular mechanism whereby the increase in BP variability aggravates hypertensive organ damages remains unknown. Thus, we created a rat chronic model of a combination of hypertension and large BP variability by performing bilateral sino-aortic denervation in spontaneously hypertensive rat. A series of our studies using this model revealed that large BP variability induces chronic myocardial inflammation by activating local angiotensin II and mineralocorticoid receptor systems and thereby aggravates cardiac hypertrophy and myocardial fibrosis, leading to systolic dysfunction, in hypertensive hearts. In addition, large BP variability induces the aggravation of arteriolosclerotic changes and ischemic cortical fibrosis in hypertensive kidney via local angiotensin II system.