Restraint stress modulates brain, pituitary and adrenal expression of angiotensin II AT1A, AT1B and AT2 receptors

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Journal Article

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Adrenal gland; Angiotensin; Angiotensin receptors; In situ hybridization; Paraventricular nucleus; Stress; Subfornical organ


Angiotensin II (Ang II) AT1 receptors are involved in the regulation of the stress response. In adult male rats, acute restraint increased AT1A mRNA in paraventricular nucleus. Repeated restraint increased AT1A mRNA and AT1 binding in paraventricular nucleus and AT1 binding in subfornical organ and median eminence. AT1B and AT2 receptors were not expressed in brain areas involved in the stress response. Acute restraint increased anterior pituitary AT1A mRNA and AT1 binding and decreased AT1B mRNA. During repeated restraint, the increase in AT1A mRNA in the anterior pituitary was maintained, but AT1B mRNA and AT1 binding returned to normal levels. In adrenal zona glomerulosa, AT1B mRNA, AT1 binding, AT2 mRNA and AT2 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 AT2 mRNA. In adrenal medulla, AT1A mRNA increased and AT2 mRNA decreased during acute restraint. AT1A mRNA remained increased during repeated restraint, while alterations in AT2 mRNA were no longer present. Expression of AT1A, AT1B and AT2 receptors in the hypothalamic-pituitary-adrenal axis is tissue specific and is different in acute and repeated stress. Increased brain, pituitary and adrenomedullary AT1A receptor expression correlates with hypothalamic-pituitary-adrenal axis stimulation, supporting the hypothesis of Ang II, through selective AT1A receptor stimulation, as an important determinant of the acute and repeated stress response. Decreased adrenal zona glomerulosa and anterior pituitary AT1B receptors during acute stress can be interpreted as compensatory to increased stimulation by Ang II. There may be additional roles for adrenal AT2 receptors during acute stress, possibly related to interaction or cross-talk with AT1 receptors. Copyright © 2002 S. Karger AG, Basel.