Involvement of central angiotensin receptors in stress adaptation

Involvement of central angiotensin receptors in stress adaptation
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DOI:
10.1016/s0306-4522(99)00206-7
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发表时间:
1999-01-01
期刊:
影响因子:
3.3
通讯作者:
Drolet, G
Drolet, G
中科院分区:
医学3区
文献类型:
--
作者:
Dumont, EC;Rafrafi, S;Drolet, G

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本研究探讨了急性和慢性神经源性应激源对两个应激相关脑核中两种不同血管紧张素受体表达的影响:下丘脑室旁核中的血管紧张素1A型受体和蓝斑核中的血管紧张素2型受体。雄性 Wistar 大鼠被分为四个实验组。前两组分别接受一次 90 分钟的急性固定或喷气压力训练。另外两组接受为期 10 天的每天 90 分钟的固定训练,在第 11 天,一组接受额外的 90 分钟的固定训练,另一组接受单次喷气压力(异型但仍是神经源性的)训练。在每组中,大鼠在应激前(0分钟)、应激后立即(90分钟)或150、180、270或360分钟以及最后一次应激开始后长期固定24小时进行灌注。在非应激动物中,血管紧张素受体亚型 1A 和血管紧张素受体亚型 2 信使 RNA 的基础表达量都很小。急性固定以及喷气压力诱导室旁核中血管紧张素受体亚型 1A 信使 RNA 表达的相似模式(时间过程和最大值)。血管紧张素受体亚型 1A 信使 RNA 表达在应激开始后 90-150 分钟增加,并在 360 分钟恢复到基础水平。慢性应激固定稍微改变了模式,但没有改变血管紧张素受体亚型1A信使RNA表达的最大值以进一步固定(同型)或喷气应激(异型)。急性固定和喷气压力训练诱导相似的蓝斑特异性血管紧张素受体亚型 2 信使 RNA 表达。该表达在压力开始后 90 分钟增加,并在至少 360 分钟内保持升高状态。慢性固定应激使血管紧张素受体亚型 2 信使 RNA 表达增加到与急性应激条件下观察到的水平相当。在同型(固定)或异型(喷气压力)条件下,新的急性暴露于神经源性应激源并没有进一步增加这些水平。这些结果表明,中枢血管紧张素受体是应激调节的目标。因此,在长期暴露于神经源性应激源期间,应激可能会调节室旁核和蓝斑的血管紧张素功能。 (C) 1999 国际广播组织。由爱思唯尔科学有限公司出版
The present study examined the effects of acute and chronic neurogenic stressors on the expression of two distinct angiotensin receptors in two stress-related brain nuclei: angiotensin type 1A receptor in the paraventricular nucleus of the hypothalamus and angiotensin type 2 receptor in the nucleus locus coeruleus. Male Wistar rats were divided into four experimental groups. The first two groups were subjected once to an acute 90-min immobilization or air-jet stress session, respectively. The other two groups were subjected to 10 days of daily 90-min immobilization sessions and, on the 11th day, one group was exposed to an additional 90-min immobilization and the other to a single air-jet stress (heterotypic but still neurogenic) session. In each group, rats were perfused before stress (0 min), immediately following stress (90 min) or 150, 180, 270 or 360 min land 24 h in chronic immobilization after the beginning of the last stress session. Basal expression of both angiotensin receptor subtype 1A and angiotensin receptor subtype 2 messenger RNA was minimal in non-stressed animals. Acute immobilization as well as air-jet stress induced similar patterns (time-course and maximal values) of angiotensin receptor subtype 1A messenger RNA expression in the paraventricular nucleus. Angiotensin receptor subtype 1A messenger RNA expression increased 90-150 min after the beginning of the stress and returned to basal levels by 360 min. Chronic stress immobilization slightly modified the pattern, but not maximal values of angiotensin receptor subtype 1A messenger RNA expression to further immobilization (homotypic) or air-jet stress (heterotypic). Acute immobilization and air-jet stress sessions induced similar locus coeruleus-specific angiotensin receptor subtype 2 messenger RNA expression. This expression increased 90 min following the onset of the stress session and remained elevated for at least 360 min. Chronic immobilization stress increased angiotensin receptor subtype 2 messenger RNA expression to levels comparable to those observed in acute stress conditions. Novel acute exposure to neurogenic stressors did not further increase these levels in either homotypic (immobilization) or in heterotypic (air-jet stress) conditions. These results suggest that central angiotensin receptors are targets of regulation in stress; therefore, stress may modulate angiotensin function in the paraventricular nucleus and locus coeruleus during chronic exposure to neurogenic stressors. (C) 1999 IBRO. Published by Elsevier Science Ltd.