Key result
Chronic mild stress significantly increased AT1a receptor mRNA expression in the brain (e.g., 1.689 vs 0.027 in septal/accumbal diencephalon, p<0.001) and kidney of male rats.
Why the study?
Does chronic mild stress increase AT1aR mRNA expression in the brain and kidney of male Sprague-Dawley rats?
Does chronic mild stress increase AT1aR mRNA expression in the brain and kidney of male Sprague-Dawley rats?
Absolute Event Rate: 1.689% vs 0.027%
p-value: p=< .001
Chronic mild stress significantly enhances the expression of the AT1aR gene in the brain and kidney of rats, suggesting a potential mechanism for stress-induced potentiation of negative effects of angiotensin II.
Potential mechanism linking stress to angiotensin II effects requires human validation; leaves open clinical relevance of AT1aR modulation.
OBJECTIVE: The purpose of the study was to determine whether exposure to chronic mild stress (CMS) affects expression of angiotensin II Type 1a receptor (AT1aR) messenger RNA (mRNA) in the brain and kidney. METHODS: Male Sprague-Dawley rats were divided into an unchallenged control group, which remained at rest, and an experimental group, exposed to CMS produced by a series of unexpected, disturbing stimuli applied at random over a period of 4 weeks. After sacrificing the animals, samples of the septal/accumbal and hypothalamic/thalamic diencephalon, brain medulla, cerebellum, and the renal medulla were harvested for determination of AT1aR mRNA. RESULTS: Expression of AT1a receptor mRNA was significantly greater in the rats in the CMS condition than in the controls (septal/accumbal diencephalon: 1.689 [0.205] versus 0.027 [0.004], hypothalamic/thalamic diencephalon: 1.239 [0.101] versus 0.003 [0.001], brain medulla: 2.694 [0.295] versus 0.028 [0.003], cerebellum: 0.013 [0.002] versus 0.005 [0.001; p < .001 for all comparisons], and renal medulla: 409.92 [46.92] versus 208.06 [30.56; p < .01]). There was a significant positive correlation between AT1a mRNA expression in the septal/accumbal diencephalon and brain medulla (p < .025). CONCLUSIONS: The results provide evidence that CMS significantly enhances expression of the AT1aR gene in the brain and kidney and indicate that changes in expression of AT1aR mRNA in different brain regions during CMS may be causally related. It is suggested that the up-regulation of AT1a receptors by chronic stress may potentiate negative effects of angiotensin II in pathologies associated with activation of the renin-angiotensin system.
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Milik et al. (2015) studied Chronic mild stress. Chronic mild stress (CMS) vs. Unchallenged control group was evaluated on Expression of angiotensin II Type 1a receptor (AT1aR) mRNA in the brain and kidney (p=< .001). Chronic mild stress significantly increased AT1a receptor mRNA expression in the brain (e.g., 1.689 vs 0.027 in septal/accumbal diencephalon, p<0.001) and kidney of male rats.
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