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Effect of Chronic Mild Stress on At1 Receptor Messenger Rna Expression in the Brain and Kidney of Rats

Bibliographic Data

ID19308293
AuthorsElwira Milik, Agnieszka Cudnoch-Jedrzejewska, Agnieszka Cudnoch‐Jędrzejewska (0000-0002-1605-4447), Ewa Szczepanska-Sadowska, Ewa Szczepańska‐Sadowska (0000-0002-3761-508X, Medical University of Warsaw, corresponding author)
Year2016
Volume78
Issue2
Pages208-220
Publication date2016-02-01
Open AccessNo
TypeARTICLE
VenuePsychosomatic Medicine (JOURNAL)
Journal identifiersISSN: 0033-3174 • E-ISSN: 1534-7796
PublisherOvid Technologies (Wolters Kluwer Health) (PUBLISHER)
DOI10.1097/psy.0000000000000269
PMID26575857
OpenAlexW2420065946
LanguageEN
References cited63

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

Angiotensin II · Angiotensin II receptor type 1 · Biology · Chronic stress · Gene · Kidney · Messenger RNA · Receptor · Second messenger system · Biochemistry · Chemistry · Endocrinology · Internal Medicine · Medicine · Neuropeptides and Animal Physiology · Renin-Angiotensin System Studies · Stress Responses and Cortisol

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