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

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          Abstract

          Angiotensin II (Ang II) AT<sub>1</sub> receptors are involved in the regulation of the stress response. In adult male rats, acute restraint increased AT<sub>1A</sub> mRNA in paraventricular nucleus. Repeated restraint increased AT<sub>1A</sub> mRNA and AT<sub>1</sub> binding in paraventricular nucleus and AT<sub>1</sub> binding in subfornical organ and median eminence. AT<sub>1B</sub> and AT<sub>2</sub> receptors were not expressed in brain areas involved in the stress response. Acute restraint increased anterior pituitary AT<sub>1A</sub> mRNA and AT<sub>1</sub> binding and decreased AT<sub>1B</sub> mRNA. During repeated restraint, the increase in AT<sub>1A</sub> mRNA in the anterior pituitary was maintained, but AT<sub>1B</sub> mRNA and AT<sub>1</sub> binding returned to normal levels. In adrenal zona glomerulosa, AT<sub>1B</sub> mRNA, AT<sub>1</sub> binding, AT<sub>2</sub> mRNA and AT<sub>2</sub> 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</sub> mRNA. In adrenal medulla, AT<sub>1A</sub> mRNA increased and AT<sub>2</sub> mRNA decreased during acute restraint. AT<sub>1A</sub> mRNA remained increased during repeated restraint, while alterations in AT<sub>2</sub> mRNA were no longer present. Expression of AT<sub>1A</sub>, AT<sub>1B</sub> and AT<sub>2</sub> 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</sub> receptor expression correlates with hypothalamic-pituitary-adrenal axis stimulation, supporting the hypothesis of Ang II, through selective AT<sub>1A</sub> receptor stimulation, as an important determinant of the acute and repeated stress response. Decreased adrenal zona glomerulosa and anterior pituitary AT<sub>1B</sub> 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</sub> receptors during acute stress, possibly related to interaction or cross-talk with AT<sub>1</sub> receptors.

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          Most cited references 4

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          Isolation of a cDNA encoding the vascular type-1 angiotensin II receptor.

          Angiotensin II is an important effector molecule controlling blood pressure and volume in the cardiovascular system. Its importance is manifested by the efficacy of angiotensin-converting enzyme inhibitors in the treatment of hypertension and congestive heart failure. Angiotensin II interacts with two pharmacologically distinct subtypes of cell-surface receptors, AT1 and AT2. AT1 receptors seem to mediate the major cardiovascular effects of angiotensin II. Here we report the isolation by expression cloning of a complementary DNA encoding a unique protein with the pharmacological specificity of a vascular AT1 receptor. Hydropathic modelling of the deduced protein suggests that it shares the seven-transmembrane-region motif with the G protein-coupled receptor superfamily. Knowledge of the AT1 receptor primary sequence should now permit structural analysis, definition of the angiotensin II receptor gene family and delineation of the contribution of AT receptors to the genetic component of hypertension.
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            The AT2 receptor: fact, fancy and fantasy.

            The angiotensin AT2 receptor subtype was recently cloned and pharmacologically characterized but its function still remains elusive and controversial. It is a member of the G-protein coupled receptor superfamily with a minimal sequence homology with the AT1 receptor, responsible for the known effect of angiotensin II. The AT2 receptor displays a totally different signaling mechanisms from the AT1 receptor and involves various phosphatases. It is expressed at low density in adult tissues but up-regulated in pathological circumstances. Clearly, the AT2 receptor has antiproliferative properties and therefore opposes the growth promoting effect linked to the AT1 receptor stimulation. It is also reported that the AT2 receptor regulates ionic fluxes, affects differentiation and nerve regeneration, has anti-angiogenic and anti-fibrotic properties and stimulates apoptosis. However, the results, although suggestive, are sometimes equivocal. Obviously, the AT2 receptor plays a role in the pathogenesis and remodeling of cardiovascular and renal diseases. A more extensive knowledge of the AT2 receptor could therefore contribute to the understanding of the clincial beneficial effects of the AT1 receptor antagonists.
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              Calibration of 125I-polymer standards with 125I-brain paste standards for use in quantitative receptor autoradiography.

              125I-Polymer standards were calibrated by interpolation of their optical densities in [125I]-brain paste standard curves to obtain dpm/mg protein. There was a linear relationship between the calibrated polymer standards and the dpm/mg polymer, as provided by the manufacturer. One dpm/mg polymer was equivalent to 7.34 +/- 0.22 dpm/mg protein. Receptor quantification in selected rat brain areas with comparison to either brain paste or calibrated polymer standards yielded similar results.
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2002
                April 2002
                17 April 2002
                : 75
                : 4
                : 227-240
                Affiliations
                Section on Pharmacology, National Institute of Mental Health, Bethesda, Md., USA
                Article
                54714 Neuroendocrinology 2002;75:227–240
                10.1159/000054714
                11979053
                © 2002 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 9, References: 57, Pages: 14
                Categories
                Corticotropin and Stress

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