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.

中文翻译：

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抑制应激诱导的高血压 ISIAH 大鼠下丘脑 Fos 及相关基因的表达

摘要

压力在动脉高血压和许多其他心血管疾病并发症中起着重要作用。人们对机体对压力影响的反应的分子机制的研究给予了相当多的关注，但在细节的理解上仍然存在许多空白。ISIAH 大鼠模拟压力敏感型动脉高血压。ISIAH 大鼠的特点是基因决定的下丘脑-垂体-肾上腺皮质和交感神经-肾上腺髓质系统的活动增强，表明应激反应性增加的功能状态。首次研究了成年雄性高血压 ISIAH 大鼠单次受到束缚应激 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转录在约束应激开始后 1 小时被激活并达到峰值。Fos激活的时间进程与应激后血压升高的时间进程一致。下丘脑神经元的激活还会改变几种转录因子基因（Jun、Nr4a3、Jdp2和Ppargc1a）的转录水平，这些基因与心血管疾病的发展相关。由于Fos诱导是脑神经元激活的标志，因此得出结论，高血压 ISIAH 大鼠在短期约束期间，下丘脑神经元的激活和血压升高伴随着下丘脑-垂体-肾上腺皮质和交感肾上腺系统的应激反应性增加。