Abstract：
Stress can play a significant role in arterial hypertension and many other complications of cardiovascular diseases. Considerable attention is paid to the study of the molecular mechanisms involved in the body response to stressful influences, but there are still many blank spots in understanding the details. ISIAH rats model the stress-sensitive form of arterial hypertension. ISIAH rats are characterized by genetically determined enhanced activities of the hypothalamic-pituitary-adrenocortical and sympathetic-adrenomedullary systems, suggesting a functional state of increased stress reactivity. For the first time, the temporal expression patterns of Fos and several related genes were studied in the hypothalamus of adult male hypertensive ISIAH rats after a single exposure to restraint stress for 30, 60, or 120 min. Fos transcription was activated and peaked 1 h after the start of restraint stress. The time course of Fos activation coincided with that of blood pressure increase after stress. Activation of hypothalamic neurons also alters the transcription levels of several transcription factor genes (Jun, Nr4a3, Jdp2, and Ppargc1a), which are associated with the development of cardiovascular diseases. Because Fos induction is a marker of brain neuron activation, activation of hypothalamic neurons and an increase in blood pressure were concluded to accompany increased stress reactivity of the hypothalamic-pituitary-adrenocortical and sympathoadrenal systems in hypertensive ISIAH rats during short-term restraint.
摘要：
压力可以在动脉高血压和许多其他心血管疾病并发症中起重要作用。相当重视对身体对压力影响的反应所涉及的分子机制的研究，但是在理解细节方面仍然有很多空白。ISIAH大鼠建立动脉高血压的应激敏感形式模型。ISIAH大鼠的特征是下丘脑-垂体-肾上腺皮质和交感神经-肾上腺髓质系统的遗传决定的活动增强，提示应激反应性增加的功能状态。第一次,研究了成年雄性高血压ISIAH大鼠在一次暴露于约束应激30、60或120分钟后下丘脑中Fos和几个相关基因的时间表达模式。Fos转录被激活，并在束缚应激开始后1小时达到峰值。Fos激活的时间过程与压力后血压升高的时间过程一致。下丘脑神经元的激活也改变了几种转录因子基因的转录水平(Jun，Nr4a3、Jdp2和Ppargc1a)，与心血管疾病的发展有关。因为Fos诱导是大脑神经元激活的标志,结论是在短期约束期间,高血压ISIAH大鼠下丘脑-垂体-肾上腺皮质和交感肾上腺系统的应激反应性增加,伴随下丘脑神经元的激活和血压的升高.
