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Restraint Stress Modulates Brain, Pituitary and Adrenal Expression of Angiotensin II AT sub(1A), AT sub(1B) and AT sub(2) Receptors
Restraint Stress Modulates Brain, Pituitary and Adrenal Expression of Angiotensin II AT sub(1A), AT sub(1B) and AT sub(2) Receptors
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Restraint Stress Modulates Brain, Pituitary and Adrenal Expression of Angiotensin II AT sub(1A), AT sub(1B) and AT sub(2) Receptors
Restraint Stress Modulates Brain, Pituitary and Adrenal Expression of Angiotensin II AT sub(1A), AT sub(1B) and AT sub(2) Receptors

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Restraint Stress Modulates Brain, Pituitary and Adrenal Expression of Angiotensin II AT sub(1A), AT sub(1B) and AT sub(2) Receptors
Restraint Stress Modulates Brain, Pituitary and Adrenal Expression of Angiotensin II AT sub(1A), AT sub(1B) and AT sub(2) Receptors
Journal Article

Restraint Stress Modulates Brain, Pituitary and Adrenal Expression of Angiotensin II AT sub(1A), AT sub(1B) and AT sub(2) Receptors

2002
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Overview
Angiotensin II (Ang II) AT sub(1) receptors are involved in the regulation of the stress response. In adult male rats, acute restraint increased AT sub(1A) mRNA in paraventricular nucleus. Repeated restraint increased AT sub(1A) mRNA and AT sub(1) binding in paraventricular nucleus and AT sub(1) binding in subfornical organ and median eminence. AT sub(1B) and AT sub(2) receptors were not expressed in brain areas involved in the stress response. Acute restraint increased anterior pituitary AT sub(1A) mRNA and AT sub(1) binding and decreased AT sub(1B) mRNA. During repeated restraint, the increase in AT sub(1A) mRNA in the anterior pituitary was maintained, but AT sub(1B) mRNA and AT sub(1) binding returned to normal levels. In adrenal zona glomerulosa, AT sub(1B) mRNA, AT sub(1) binding, AT sub(2) mRNA and AT sub(2) binding decreased during acute restraint. Receptor mRNA and binding returned to normal after repeated stress, with the exception of rebound increase in adrenal zona glomerulosa AT sub(2) mRNA. In adrenal medulla, AT sub(1A) mRNA increased and AT sub(2) mRNA decreased during acute restraint. AT sub(1A) mRNA remained increased during repeated restraint, while alterations in AT sub(2) mRNA were no longer present. Expression of AT sub(1A), AT sub(1B) and AT sub(2) receptors in the hypothalamic-pituitary-adrenal axis is tissue specific and is different in acute and repeated stress. Increased brain, pituitary and adrenomedullary AT sub(1A) receptor expression correlates with hypothalamic-pituitary-adrenal axis stimulation, supporting the hypothesis of Ang II, through selective AT sub(1A) receptor stimulation, as an important determinant of the acute and repeated stress response. Decreased adrenal zona glomerulosa and anterior pituitary AT sub(1B) receptors during acute stress can be interpreted as compensatory to increased stimulation by Ang II. There may be additional roles for adrenal AT sub(2) receptors during acute stress, possibly related to interaction or cross-talk with AT sub(1) receptors.

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