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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

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      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

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      Nongenomic Effects of Aldosterone on Renal Protein Expressions of pEGFR and pERK1/2 in Rat Kidney

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          Abstract

          Background: In vitro studies have demonstrated that aldosterone elicits nongenomic actions by enhancing protein expressions of phosphorylated epidermal growth factor receptor (pEGFR) and phosphorylated extracellular signal-regulated kinases 1/2 (pERK1/2). There are no available in vivo investigations regarding this action of aldosterone on renal pEGFR-pERK1/2 protein expressions. Methods: Male Wistar rats received normal saline solution, low-dose (LA: 150 µg/kg BW) or high-dose aldosterone (HA: 500 µg/kg BW) by intraperitoneal injection. After 30 min, protein abundances and localizations of renal pEGFR and pERK1/2 were determined by Western blot and immunohistochemistry. Results: Plasma aldosterone levels were increased in LA and HA groups (p < 0.001). Aldosterone enhanced renal pEGFR and pERK1/2 protein abundances (p < 0.001). HA showed a greater stimulation on pEGFR immunoreactivity than LA in the glomerulus, vasa recta, and thin limb of Henle’s loop in the inner medulla area. LA provided more reactivity of pERK1/2 in the thick ascending limb of Henle’s loop, outer medullary collecting duct, and proximal straight tubule, whereas HA illustrated more pERK1/2 activation in the glomerulus, peritubular capillary, and inner medulla region. Conclusion: This is the first in vivo study which demonstrates that aldosterone, via the nongenomic pathway, could elevate pEGFR and pERK1/2 protein abundances and expressions in the rat kidney. These results indicate that aldosterone induces phosphorylation of EGFR upstream of ERK1/2.

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          The new biology of aldosterone.

          John M C Connell, Eleanor Davies (2005)
          Classically, aldosterone is synthesised in the adrenal zona glomerulosa and binds to specific mineralocorticoid receptors located in the cytosol of target epithelial cells. Translocation of the resulting steroid receptor complex to the cell nucleus modulates gene expression and translation of specific 'aldosterone-induced' proteins that regulate electrolyte and fluid balance. However, non-epithelial and rapid non-genomic actions of aldosterone have also been described that account for a variety of actions of aldosterone that contribute to blood pressure homeostasis. These include key actions on endothelial cells and on cardiac tissue. There is also evidence that aldosterone can be synthesised in other tissues; the most convincing evidence relates to the central nervous system. However, suggestions that aldosterone is produced in the heart remain controversial, and adrenal derived aldosterone is the principal source of circulating and locally available hormone. Recent studies have shown major therapeutic benefits of mineralocorticoid receptor antagonism in cardiac failure, which emphasise the importance of aldosterone in causing adverse cardiovascular pathophysiological effects. Additional evidence demonstrates that aldosterone levels predict development of high blood pressure in normotensive subjects, while it is now clear that increased aldosterone action contributes to hypertension and cardiovascular damage in approximately 10% of patients with established hypertension. These new findings highlight the role of aldosterone as a key cardiovascular hormone and extend our understanding of its role in determining adverse cardiovascular outcomes.
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            Aldosterone regulates vascular reactivity: short-term effects mediated by phosphatidylinositol 3-kinase-dependent nitric oxide synthase activation.

            Selina L Liu, Saskia Schmuck, Jozef Chorazcyzewski … (2003)
            There is increasing evidence for rapid nongenomic effects of aldosterone. Therefore, we studied the immediate effects of aldosterone on vascular reactivity in rat aortic ring segments and on endothelial and vascular smooth muscle cellular responses. In endothelium-intact ring segments, aldosterone attenuated phenylephrine-mediated constriction (maximal reduction, 25+/-4% below control phenylephrine-mediated constriction). In contrast, in endothelium-denuded vessels, aldosterone mediated a monophasic dose-dependent enhancement of vasoconstrictor response. In endothelial cells, aldosterone caused a phosphatidylinositol 3-kinase (PI3K)-dependent increase in nitric oxide synthase activity as well as PI3K-dependent activation of extracellular signal-regulated kinase 1/2 and p70 S6 kinase. Overall, these data support a novel effect of aldosterone on vascular endothelial and smooth muscle cell function. These rapid effects of aldosterone might be important in both the short- and long-term regulation of peripheral vascular resistance. Furthermore, in the setting of endothelial dysfunction, alterations in aldosterone's short-term vascular responses might contribute to its pathophysiological effects in cardiovascular disease.
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              New aspects of rapid aldosterone signaling.

              M Gekle, C Grossmann (2009)
              Aldosterone, the endogenous ligand of the mineralocorticoid receptor (MR) in humans, is a steroid hormone that regulates salt and water homeostasis. Recently, additional pathophysiological effects in the renocardiovascular system have been identified. Besides genomic effects mediated by activated MR, rapid aldosterone actions that are independent of translation and transcription have been documented. While these nongenomic actions influence electrolyte homeostasis, pH and cell volume in classical MR target organs, they also participate in pathophysiological effects in the renocardiovascular system causing endothelial dysfunction, inflammation and remodeling. The mechanisms conveying these rapid effects consist of a multitude of signaling molecules and include a cross-talk with genomic aldosterone effects as well as with angiotensin II and epidermal growth factor receptor signaling. Rapid corticosteroid signaling via the MR has also been demonstrated in the brain. Altogether, the function of nongenomic aldosterone effects seems to be to modulate other signaling cascades, depending on the surrounding milieu.
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                Author and article information

                Journal
                Journal ID (publisher-id): AJN
                Journal ID (nlm-ta): Am J Nephrol
                Journal ID (doi): 10.1159/issn.0250-8095
                Title: American Journal of Nephrology
                Publisher: S. Karger AG
                ISSN (Print): 0250-8095
                ISSN (Electronic): 1421-9670
                Publication date Subscription-year: 2011
                Publication date (Print): March 2011
                Publication date (Electronic): 22 December 2010
                Volume: 33
                Issue: 2
                Pages: 111-120
                Affiliations
                aInter-Department of Physiology, Graduate School, bDepartment of Physiology, and cDivision of Nephrology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, and dDepartment of Medicine, Lerdsin General Hospital, Bangkok, Thailand
                Author notes
                *Assoc. Prof. Somchit Eiam-Ong, PhD, Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330 (Thailand), Tel./Fax +66 2 256 4267, E-Mail EiamOng@netscape.net
                Article
                Publisher ID: 322965 Other ID: Am J Nephrol 2011;33:111–120
                DOI: 10.1159/000322965
                PubMed ID: 21196724
                SO-VID: c1cd06ef-0073-4865-bcd2-62d9a2c213f7
                Copyright © © 2010 S. Karger AG, Basel
                License:

                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.

                History
                Date received : 20 September 2010
                Date accepted : 20 November 2010
                Page count
                Figures: 6, Tables: 2, Pages: 10
                Categories
                Subject: Original Report: Laboratory Investigation

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Nongenomic action,Aldosterone,Rat kidney,Protein abundance,Immunohistochemistry,pEGFR-pERK1/2
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Nongenomic action, Aldosterone, Rat kidney, Protein abundance, Immunohistochemistry, pEGFR-pERK1/2

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